tag:theconversation.com,2011:/ca-fr/topics/virology-6639/articlesVirology – La Conversation2024-01-25T20:46:49Ztag:theconversation.com,2011:article/2202852024-01-25T20:46:49Z2024-01-25T20:46:49ZThe emergence of JN.1 is an evolutionary ‘step change’ in the COVID pandemic. Why is this significant?<figure><img src="https://images.theconversation.com/files/571359/original/file-20240125-15-2lt45r.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C7667%2C3900&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/evolution-covid19-sarscov2-mutating-coronavirus-virus-2344854903">Lightspring/Shutterstock</a></span></figcaption></figure><p>Since it was detected in <a href="https://www.gavi.org/vaccineswork/seven-things-you-need-know-about-jn1-covid-19-variant">August 2023</a>, the JN.1 variant of COVID has <a href="https://news.un.org/en/story/2023/12/1145012">spread widely</a>. It has become dominant in Australia and <a href="https://outbreak.info/situation-reports?xmin=2023-07-05&xmax=2024-01-05&pango=JN.1">around the world</a>, driving the <a href="https://www.cdc.gov/respiratory-viruses/whats-new/JN.1-update-2024-01-05.html">biggest COVID wave</a> seen in many jurisdictions for at least the past year.</p>
<p>The World Health Organization (WHO) <a href="https://news.un.org/en/story/2023/12/1145012">classified</a> JN.1 as a “variant of interest” in December 2023 and in January <a href="https://x.com/UNGeneva/status/1745782729558348212?s=20">strongly stated</a> COVID was a continuing global health threat causing “far too much” preventable disease with worrying potential for long-term health consequences. </p>
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<p>JN.1 is significant. First as a pathogen – it’s a surprisingly new-look version of SARS-CoV-2 (the virus that causes COVID) and is rapidly displacing other circulating strains (omicron XBB). </p>
<p>It’s also significant because of what it says about COVID’s evolution. Normally, SARS-CoV-2 variants look quite similar to what was there before, accumulating just a few mutations at a time that give the virus a meaningful advantage over its parent. </p>
<p>However, occasionally, as was the case when omicron (B.1.1.529) arose two years ago, variants emerge seemingly out of the blue that have markedly different characteristics to what was there before. This has significant implications for disease and transmission. </p>
<p>Until now, it wasn’t clear this “step-change” evolution would happen again, especially given the ongoing success of the steadily evolving omicron variants. </p>
<p>JN.1 is so distinct and causing such a wave of new infections that many are wondering whether the <a href="https://www.who.int/activities/tracking-SARS-CoV-2-variants">WHO</a> will recognise JN.1 as the next variant of concern with its own Greek letter. In any case, with JN.1 we’ve entered a new phase of the pandemic.</p>
<h2>Where did JN.1 come from?</h2>
<p>The JN.1 (or BA.2.86.1.1) story begins with the emergence of its <a href="https://erictopol.substack.com/p/from-a-detour-to-global-dominance">parent lineage</a> BA.2.86 around mid 2023, which originated from a much earlier (2022) omicron sub-variant BA.2.</p>
<p><a href="https://www.nature.com/articles/d41586-022-01613-2">Chronic infections</a> that may linger unresolved for months (if not years, in some people) likely play a role in the emergence of these step-change variants. </p>
<p>In chronically infected people, the virus silently tests and eventually retains many mutations that help it avoid immunity and survive in that person. For BA.2.86, this resulted in <a href="https://theconversation.com/how-evasive-and-transmissible-is-the-newest-omicron-offshoot-ba-2-86-that-causes-covid-19-4-questions-answered-212453">more than 30 mutations</a> of the spike protein (a protein on the surface of SARS-CoV-2 that allows it to attach to our cells). </p>
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Read more:
<a href="https://theconversation.com/covid-is-surging-in-australia-and-only-1-in-5-older-adults-are-up-to-date-with-their-boosters-220839">COVID is surging in Australia – and only 1 in 5 older adults are up to date with their boosters</a>
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<p>The sheer volume of infections occurring globally sets the scene for major viral evolution. SARS-CoV-2 continues to have a <a href="https://nextstrain.org/ncov/gisaid/global/all-time?dmin=2021-04-07&l=clock">very high rate of mutation</a>. Accordingly, JN.1 itself is already <a href="https://twitter.com/dfocosi/status/1744982175508771190">mutating and evolving</a> quickly.</p>
<h2>How is JN.1 different to other variants?</h2>
<p>BA.2.86 and now JN.1 are behaving in a manner that looks unique in laboratory studies in two ways.</p>
<p>The first relates to how the virus evades immunity. JN.1 has inherited <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(23)00813-7/fulltext#%20">more than 30 mutations</a> in its spike protein. It also acquired a new mutation, <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(23)00744-2/fulltext">L455S</a>, which further decreases the ability of antibodies (one part of the immune system’s protective response) to bind to the virus and prevent infection.</p>
<p>The second involves changes to the way JN.1 <a href="https://www.nature.com/articles/s41580-021-00418-x">enters</a> and replicates in our cells. Without delving in to the molecular details, recent high-profile lab-based research from the <a href="https://www.cell.com/action/showPdf?pii=S0092-8674%2823%2901400-9">United States</a> and <a href="https://www.cell.com/action/showPdf?pii=S0092-8674%2823%2901399-5">Europe</a> observed BA.2.86 to enter cells from the lung in a similar way to pre-omicron variants like delta. However, in contrast, preliminary work by Australia’s Kirby Institute <a href="https://www.biorxiv.org/content/10.1101/2023.09.22.558930v2">using different techniques</a> finds replication characteristics that are aligned better with omicron lineages. </p>
<p>Further research to resolve these different cell entry findings is important because it has implications for where the virus may prefer to replicate in the body, which could affect disease severity and transmission. </p>
<p>Whatever the case, these findings show JN.1 (and SARS-CoV-2 in general) can not only navigate its way around our immune system, but is finding new ways to infect cells and transmit effectively. We need to further study how this plays out in people and how it affects clinical outcomes.</p>
<h2>Is JN.1 more severe?</h2>
<figure class="align-center ">
<img alt="A woman in a supermarket wearing a mask." src="https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/571362/original/file-20240125-17-9zn8rj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">JN.1 has some characteristics which distinguish it from other variants.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/alarmed-female-wears-medical-mask-against-1708365295">Elizaveta Galitckaia/Shutterstock</a></span>
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<p>The step-change evolution of BA.2.86, combined with the immune-evading features in JN.1, has given the virus a <a href="https://www.who.int/docs/default-source/coronaviruse/18122023_jn.1_ire_clean.pdf?sfvrsn=6103754a_3">global growth advantage</a> well beyond the XBB.1-based lineages we faced in 2023. </p>
<p>Despite these features, evidence suggests our <a href="https://www.news-medical.net/news/20231208/T-cells-can-recognize-and-fight-the-Pirola-variant-new-study-suggests.aspx">adaptive immune system</a> could still recognise and respond to BA.286 and JN.1 effectively. Updated monovalent vaccines, tests and treatments <a href="https://publichealth.jhu.edu/2024/jn1-the-dominant-variant-in-the-covid-surge">remain effective</a> against JN.1. </p>
<p>There are two elements to “severity”: first if it is more “intrinsically” severe (worse illness with an infection in the absence of any immunity) and second if the virus has greater transmission, causing greater illness and deaths, simply because it infects more people. The latter is certainly the case with JN.1. </p>
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Read more:
<a href="https://theconversation.com/how-long-does-immunity-last-after-a-covid-infection-221398">How long does immunity last after a COVID infection?</a>
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<h2>What next?</h2>
<p>We simply don’t know if this virus is on an evolutionary track to becoming the “next common cold” or not, nor have any idea of what that timeframe might be. While <a href="https://www.science.org/content/article/four-cold-causing-coronaviruses-may-provide-clues-covids-future">examining the trajectories</a> of four historic coronaviruses could give us a glimpse of where we may be heading, this should be considered as just one possible path. The emergence of JN.1 underlines that we are experiencing a continuing epidemic with COVID and that looks like the way forward for the foreseeable future. </p>
<p>We are now in a new pandemic phase: post-emergency. Yet COVID remains the major infectious disease causing harm globally, from both acute infections and <a href="https://theconversation.com/long-covid-symptoms-can-improve-but-their-resolution-is-slow-and-imperfect-212015">long COVID</a>. At a societal and an individual level we need to re-think the risks of accepting wave after wave of infection. </p>
<p>Altogether, this underscores the importance of <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)01585-9/fulltext">comprehensive strategies to reduce COVID transmission and impacts</a>, with the least imposition (such as <a href="https://www.mja.com.au/journal/2022/217/11/healthy-indoor-air-our-fundamental-need-time-act-now">clean indoor air interventions</a>). </p>
<p>People are <a href="https://www.health.vic.gov.au/health-alerts/increase-in-covid-19-cases">advised</a> to continue to take active steps to protect themselves and those around them. </p>
<p>For better pandemic preparedness for emerging threats and an improved response to the current one it is crucial we <a href="https://www.who.int/publications/m/item/virtual-press-conference-on-global-health-issues-transcript-10-january-2024">continue global surveillance</a>. The low representation of low- and middle- income countries is a concerning blind-spot. Intensified research is also crucial.</p><img src="https://counter.theconversation.com/content/220285/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Suman Majumdar, through the Burnet Institute receives grant funding from the Australian Government via the National Health & Medical Research Council of Australia, the Medical Research Future Fund and DFAT's Centre for Health Security.</span></em></p><p class="fine-print"><em><span>Brendan Crabb and the Institute he leads receives research grant funding from the National Health & Medical Research Council of Australia, the Medical Research Future Fund, DFAT's Centre for Health Security and other Australian federal and Victorian State Government bodies. He is the Chair of The Australian Global Health Alliance and the Pacific Friends of Global Health, both in an honorary capacity. And he serves on the Board of the Telethon Kids Institute, on advisory committees of mRNA Victoria, the Sanger Institute (UK), the Institute for Health Transformation (at Deakin University), The Brain Cancer Centre (Australia), the WHO Malaria Vaccine Advisory Committee; MALVAC, and is a member of OzSAGE and The John Snow Project, all honorary positions.</span></em></p><p class="fine-print"><em><span>Stuart Turville receives funding from NHMRC through an Ideas Grant and MRFF grant related to SARS CoV-2 immunology. </span></em></p><p class="fine-print"><em><span>Emma Pakula does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The JN.1 variant has become dominant in Australia and around the world, causing large waves of infections. Here’s what we know about it so far – and why it’s so important.Suman Majumdar, Associate Professor and Chief Health Officer - COVID and Health Emergencies, Burnet InstituteBrendan Crabb, Director and CEO, Burnet InstituteEmma Pakula, Senior Research and Policy Officer, Burnet InstituteStuart Turville, Associate Professor, Immunovirology and Pathogenesis Program, Kirby Institute, UNSW SydneyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2173792024-01-09T19:15:56Z2024-01-09T19:15:56ZViruses aren’t always harmful. 6 ways they’re used in health care and pest control<figure><img src="https://images.theconversation.com/files/564112/original/file-20231207-20-amgv6b.jpg?ixlib=rb-1.1.0&rect=33%2C67%2C5573%2C3665&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/male-nurse-pushing-stretcher-gurney-bed-156022646">Shutterstock</a></span></figcaption></figure><p>We tend to just think of viruses in terms of their damaging impacts on human health and lives. <a href="https://blogs.cdc.gov/publichealthmatters/2018/05/1918-flu/">The 1918 flu pandemic</a> killed around 50 million people. <a href="https://www.cdc.gov/smallpox/about/index.html">Smallpox</a> claimed 30% of those who caught it, and survivors were often scarred and blinded. More recently, we’re all too familiar with the health and economic impacts of COVID. </p>
<p>But viruses can also be used to benefit human health, agriculture and the environment. </p>
<p>Viruses are comparatively simple in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150055/">structure</a>, consisting of a piece of genetic material (RNA or DNA) enclosed in a protein coat (the capsid). Some also have an outer envelope. </p>
<p>Viruses get into your cells and use your cell machinery to copy themselves.
Here are six ways we’ve harnessed this for health care and pest control. </p>
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Read more:
<a href="https://theconversation.com/how-do-viruses-get-into-cells-their-infection-tactics-determine-whether-they-can-jump-species-or-set-off-a-pandemic-216139">How do viruses get into cells? Their infection tactics determine whether they can jump species or set off a pandemic</a>
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<h2>1. To correct genes</h2>
<p>Viruses are used in some gene therapies to correct <a href="https://www.mdpi.com/1999-4915/15/3/698#">malfunctioning genes</a>. <a href="https://www.genome.gov/genetics-glossary/Gene">Genes</a> are DNA sequences that code for a particular protein required for cell function. </p>
<p>If we remove viral genetic material from the capsid (protein coat) we can use the space to transport a “cargo” into cells. These modified viruses are called “<a href="https://www.nature.com/articles/s41392-021-00487-6">viral vectors</a>”. </p>
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<img alt="" src="https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=401&fit=crop&dpr=1 600w, https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=401&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=401&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=504&fit=crop&dpr=1 754w, https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=504&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/564099/original/file-20231207-15-g0knkm.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=504&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Viruses consist of a piece of RNA or DNA enclosed in a protein coat called the capsid.</span>
<span class="attribution"><a class="source" href="https://en.wikipedia.org/wiki/Introduction_to_viruses#/media/File:Basic_Scheme_of_Virus_en.svg">DEXi</a></span>
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<p>Viral vectors can <a href="https://www.nature.com/articles/s41392-021-00487-6">deliver a functional gene</a> into someone with a genetic disorder whose own gene is not working properly. </p>
<p>Some <a href="https://www.mdpi.com/1999-4915/15/3/698#">genetic diseases</a> treated this way include haemophilia, sickle cell disease and beta thalassaemia. </p>
<h2>2. Treat cancer</h2>
<p>Viral vectors can be used to treat cancer. </p>
<p>Healthy people have p53, a tumour-suppressor gene. About <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884858/">half</a> of cancers are associated with the loss of p53. </p>
<p>Replacing the damaged p53 gene using a viral vector stops the cancerous cell from replicating and tells it to suicide (<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3756401/">apoptosis</a>). </p>
<p>Viral vectors can also be used to deliver an <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884858/">inactive drug</a> to a tumour, where it is then activated to kill the tumour cell. </p>
<p>This targeted therapy reduces the side effects otherwise seen with cytotoxic (cell-killing) drugs. </p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/Q6qk6Wh6cXU?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Here’s how treatment, called gene therapy, works.</span></figcaption>
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<p>We can also use <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9888358/">oncolytic</a> (cancer cell-destroying) viruses to treat some types of cancer. </p>
<p>Tumour cells have often lost their antiviral defences. In the case of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8884858/">melanoma</a>, a modified herpes simplex virus can kill rapidly dividing melanoma cells while largely leaving non-tumour cells alone. </p>
<h2>3. Create immune responses</h2>
<p>Viral vectors can create a protective immune response to a particular viral antigen. </p>
<p>One <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9317404/">COVID vaccine</a> uses a modified chimp adenovirus (adenoviruses cause the common cold in humans) to transport RNA coding for the SARS-CoV-2 spike protein into human cells. </p>
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Read more:
<a href="https://theconversation.com/how-the-puzzle-of-viral-vector-vaccines-was-solved-leading-to-todays-covid-19-shots-167341">How the puzzle of viral vector vaccines was solved, leading to today’s COVID-19 shots</a>
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<p>The RNA is then used to make spike protein copies, which stimulate our immune cells to replicate and “remember” the spike protein. </p>
<p>Then, when you are exposed to SARS-CoV-2 for real, your immune system can churn out lots of antibodies and virus-killing cells very quickly to prevent or reduce the severity of infection. </p>
<h2>4. Act as vaccines</h2>
<p>Viruses can be modified to act directly as vaccines themselves <a href="https://www.hhs.gov/immunization/basics/types/index.html">in several ways</a>. </p>
<p>We can weaken a virus (for an attenuated virus vaccine) so it doesn’t cause infection in a healthy host but can still replicate to stimulate the immune response. The chickenpox vaccine works like this. </p>
<p>The Salk vaccine for polio uses a whole virus that has been inactivated (so it can’t cause disease). </p>
<p>Others use a small part of the virus such as a capsid protein to stimulate an immune response (subunit vaccines). </p>
<p>An mRNA vaccine packages up viral RNA for a specific protein that will stimulate an immune response. </p>
<h2>5. Kill bacteria</h2>
<p>Viruses can – in limited situations <a href="https://phage.directory/capsid/phage-therapy-regulation-australia">in Australia</a> – be used to treat antibiotic-resistant bacterial infections.</p>
<p><a href="https://www.ncbi.nlm.nih.gov/books/NBK493185/">Bacteriophages</a> are viruses that kill bacteria. Each type of phage usually infects a particular species of bacteria. </p>
<p>Unlike antibiotics – which often kill “good” bacteria along with the disease-causing ones – phage therapy leaves your normal flora (useful microbes) intact. </p>
<figure class="align-center ">
<img alt="A phage" src="https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/564113/original/file-20231207-19-7ruzur.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=566&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Bacteriophages (red) are viruses that kill bacteria (green).</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/bacteriophages-viruses-that-attack-infect-bacteria-1391256956">Shutterstock</a></span>
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<h2>6. Target plant, fungal or animal pests</h2>
<p>Viruses can be species-specific (infecting one species only) and even cell-specific (infecting one type of cell only). </p>
<p>This occurs because the proteins viruses use to attach to cells have a shape that binds to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083867/#">a specific type of cell receptor</a> or molecule, like a specific key fits a lock. </p>
<p>The virus can enter the cells of all species with this receptor/molecule. For example, <a href="https://www.cdc.gov/rabies/animals/index.html">rabies virus</a> can infect all mammals because we share the right receptor, and mammals have other characteristics that allow infection to occur whereas other non-mammal species don’t. </p>
<p>When the receptor is only found on one cell type, then the virus will infect that cell type, which may only be found in one or a limited number of species. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5869238/">Hepatitis B virus</a> successfully infects liver cells primarily in humans and chimps. </p>
<p>We can use that property of specificity to target <a href="https://pubmed.ncbi.nlm.nih.gov/37682594/">invasive plant species</a> (reducing the need for chemical herbicides) and pest insects (reducing the need for chemical insecticides). <a href="https://www.tandfonline.com/doi/full/10.1080/23311932.2023.2254139">Baculoviruses</a>, for example, are used to control caterpillars. </p>
<p>Similarly, <a href="https://www.ncbi.nlm.nih.gov/books/NBK493185/">bacteriophages</a> can be used to control bacterial <a href="https://www.annualreviews.org/doi/full/10.1146/annurev-phyto-021621-114208">tomato and grapevine diseases</a>. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/phage-therapy-could-treat-some-drug-resistant-superbug-infections-but-comes-with-unique-challenges-207025">'Phage therapy' could treat some drug-resistant superbug infections, but comes with unique challenges</a>
</strong>
</em>
</p>
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<p>Other viruses reduce plant damage from <a href="https://www.annualreviews.org/doi/full/10.1146/annurev-phyto-021621-114208">fungal pests</a>. </p>
<p><a href="https://csiropedia.csiro.au/myxomatosis-to-control-rabbits/">Myxoma virus and calicivirus</a> reduce rabbit populations and their environmental impacts and improve agricultural production. </p>
<p>Just like humans can be protected against by vaccination, plants can be “<a href="https://www.annualreviews.org/doi/full/10.1146/annurev-phyto-021621-114208">immunised</a>” against a disease-causing virus by being exposed to a milder version.</p><img src="https://counter.theconversation.com/content/217379/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Thea van de Mortel teaches into the Master of Infection Prevention and Control program at Griffith University. </span></em></p>We tend to just think of viruses in terms of their damaging impacts on human health and lives. But viruses can also be used to benefit human health, agriculture and the environment.Thea van de Mortel, Professor, Nursing, School of Nursing and Midwifery, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2161392023-11-21T13:26:58Z2023-11-21T13:26:58ZHow do viruses get into cells? Their infection tactics determine whether they can jump species or set off a pandemic<figure><img src="https://images.theconversation.com/files/560185/original/file-20231117-23-zg89fr.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2309%2C1299&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Surface proteins on a virus enable it to attach to and get inside a cell to start replicating.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/new-omicron-sub-variant-bq-1-1-royalty-free-image/1435658319">koto_feja/E+ via Getty Images</a></span></figcaption></figure><p>COVID-19, flu, mpox, noroviral diarrhea: How do the viruses that cause these diseases actually infect you?</p>
<p>Viruses <a href="https://www.khanacademy.org/science/biology/biology-of-viruses/virus-biology/a/intro-to-viruses">cannot replicate on their own</a>, so they must infect cells in your body to make more copies of themselves. The life cycle of a virus can thus be roughly described as: get inside a cell, make more virus, get out, repeat. </p>
<p>Getting inside a cell, or <a href="https://doi.org/10.1016/j.jmb.2018.03.034">viral entry</a>, is the part of the cycle that most vaccines target, as well as a key barrier for viruses jumping from one species to another. <a href="https://scholar.google.com/citations?user=OQ7vzu0AAAAJ&hl=en">My lab</a> and many others study this process to better anticipate and combat emerging viruses.</p>
<h2>How viruses enter cells</h2>
<p>Different viruses travel into the body in <a href="https://www.oregon.gov/oha/ph/diseasesconditions/communicabledisease/pages/transmission.aspx">various ways</a> – via airborne droplets, on food, through contact with mucous membranes or through injection. They typically first infect host cells near their site of entry – the cells lining the respiratory tract for most airborne viruses – then either remain there or spread throughout the body.</p>
<p>Viruses <a href="https://doi.org/10.1016/j.jmb.2018.06.024">recognize specific proteins or sugars</a> on host cells and stick to them. Each virus gets only one shot at putting its genome inside a cell – if their entry machinery misfires, they risk becoming inactivated. So they <a href="https://doi.org/10.1016/j.virol.2015.02.037">use several mechanisms</a> to prevent triggering entry prematurely.</p>
<p>After the virus binds to the cell, specific molecules on the cell’s surface or within the cell’s recycling machinery <a href="https://doi.org/10.1111/tra.12389">activate viral coat proteins for entry</a>. An example is the SARS-CoV-2 spike that COVID-19 vaccines target. These proteins need to modify the cell membrane to allow the viral genome to get through without killing the cell in the process. Different viruses use different tricks for this, but most work like cellular secretion – how cells release materials into their environment – in reverse. Specialized viral proteins help <a href="https://doi.org/10.1146/annurev-virology-111821-093413">merge the membranes of the virus and the cell</a> together and release the viral core into the interior of the cell.</p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/i__QSjC-pt0?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">This animation depicts HIV fusing its membrane with a cell in order to release its contents inside.</span></figcaption>
</figure>
<p>At this point, the viral genome can enter the cell and <a href="https://doi.org/10.1016%2FB978-0-12-800947-5.00004-1">start replicating</a>. Some viruses use only the cell’s machinery to replicate, while others carry along portions of their own replication machinery and borrow some parts from the cell. After replicating their genomes, viruses assemble the components required to make new viruses.</p>
<p>Two central questions scientists are studying about viral entry are how your body’s defenses can disrupt it and what determines whether a virus from other species can infect people.</p>
<h2>Immune defenses against viruses</h2>
<p>Your body has a multilayered defense system against viral threats. But the part of your immune system called the <a href="https://doi.org/10.1016/j.jaci.2009.12.980">antibody response</a> is generally thought to be most effective at <a href="https://doi.org/10.1016/j.immuni.2022.10.017">sterilizing immunity</a> – preventing an infection from taking hold in the first place as opposed to just limiting its scope and severity. </p>
<p>For many viruses, antibodies target the part of the virus that binds to cells. This is the case not just for current COVID-19 vaccines but also the majority of immunity against influenza, whether from vaccines or from prior infection. </p>
<p>However, some antibodies target the entry machinery instead: Rather than preventing the virus from sticking, they prevent the virus from working altogether. Such antibodies are often harder for the viruses to escape from but are difficult to reproduce with vaccines. For that reason, developing antibodies that inhibit cell entry has the been the goal of many <a href="https://doi.org/10.1016/j.coviro.2016.02.002">next-generation vaccine efforts</a>.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram of the mechanisms of four classes of HIV antivirals" src="https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=496&fit=crop&dpr=1 600w, https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=496&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=496&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=623&fit=crop&dpr=1 754w, https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=623&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/551885/original/file-20231003-25-cv0pnn.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=623&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">This diagram shows how four different classes of antiviral drugs inhibit HIV. One stops viruses from entering cells, and three inhibit different viral enzymes.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:HIV-drug-classes.svg">Thomas Splettstoesser/Wikimedia Commons</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<h2>Species-hopping and pandemics</h2>
<p>The other key question researchers are asking about viral entry is <a href="https://www.cdc.gov/flu/pandemic-resources/national-strategy/risk-assessment.htm">how to tell when</a> a virus from another species poses a threat to people. This is particularly important because many viruses are first identified in animals such as bats, birds and pigs before they spread to humans, but it’s unclear which ones may cause a pandemic.</p>
<p>The part of viruses that stick to human cells varies the most across species, while the part that gets the virus into cells <a href="https://doi.org/10.1016/bs.aivir.2016.08.004">tends to stay mostly the same</a>. Many researchers have thought that viruses changing in ways that bind better to human cells, like influenza viruses that bind to cells in the nose and throat, are some of the most important warning signs for pandemic risk. </p>
<p>However, coronaviruses – the family of viruses containing SARS-CoV-2 – are prompting re-examination of that idea. This is because several animal coronaviruses can actually <a href="https://doi.org/10.1038/s41564-020-0688-y">bind to human cells</a>, but only a few seem to be able to transmit well between people.</p>
<p>Only time will tell whether researchers need to broaden their pandemic prevention horizons or if their current prioritization of risky viruses is correct. The one grim reality of pandemic research, like earthquake research, is that there will always be another one – we just don’t know when or where, and we <a href="https://www.niaid.nih.gov/sites/default/files/pandemic-preparedness-plan.pdf">want to be ready</a>.</p><img src="https://counter.theconversation.com/content/216139/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Peter Kasson receives funding from the National Institutes of Health, the National Science Foundation, the Commonwealth Health Research Board, and the Knut and Alice Wallenberg Foundation. He is affiliated with the University of Virginia, Uppsala University, and Georgia Institute of Technology.</span></em></p>Viruses can get into cells in several ways. Figuring out how to stop them from entering in the first place is a key to developing better vaccines and stopping future pandemics.Peter Kasson, Professor of Molecular Physiology and Biomedical Engineering, University of VirginiaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2163442023-11-03T12:45:40Z2023-11-03T12:45:40ZVampire viruses prey on other viruses to replicate themselves − and may hold the key to new antiviral therapies<figure><img src="https://images.theconversation.com/files/557327/original/file-20231102-23-pcztem.png?ixlib=rb-1.1.0&rect=0%2C0%2C4306%2C1431&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The satellite virus MiniFlayer (purple) infects cells by attaching itself to the neck of its helper virus, MindFlayer (gray). </span> <span class="attribution"><a class="source" href="https://doi.org/10.1038/s41396-023-01548-0">Tagide deCarvalho</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>Have you ever wondered whether the virus that gave you a nasty cold can catch one itself? It may comfort you to know that, yes, viruses can actually get sick. Even better, as karmic justice would have it, the culprits turn out to be other viruses.</p>
<p>Viruses can get sick in the sense that their normal function is impaired. When a virus enters a cell, it can either <a href="https://theconversation.com/viruses-may-be-watching-you-some-microbes-lie-in-wait-until-their-hosts-unknowingly-give-them-the-signal-to-start-multiplying-and-kill-them-189949">go dormant or start replicating right away</a>. When replicating, the virus essentially commandeers the molecular factory of the cell to make lots of copies of itself, then breaks out of the cell to set the new copies free.</p>
<p>Sometimes a virus enters a cell only to find that its new temporary dwelling is already home to another dormant virus. Surprise, surprise. What follows is a battle for control of the cell that can be won by either party. </p>
<p>But sometimes a virus will enter a cell to find a particularly nasty shock: a viral tenant waiting specifically to prey on the incoming virus.</p>
<p>I am a <a href="https://scholar.google.com/citations?user=T1I1sNAAAAAJ&hl=en">bioinformatician</a>, and <a href="https://erilllab.umbc.edu/">my laboratory</a> studies the evolution of viruses. We frequently run into “viruses of viruses,” but we recently discovered something new: a virus that <a href="https://doi.org/10.1038/s41396-023-01548-0">latches onto the neck of another virus</a>.</p>
<h2>A world of satellites</h2>
<p>Biologists have known of the existence of viruses that prey on other viruses – referred to as <a href="https://doi.org/10.1038/nrmicro2676">viral “satellites”</a> – for decades. In 1973, researchers studying bacteriophage P2, a virus that infects the gut bacterium <em>Escherichia coli</em>, found that this infection sometimes led to two different types of viruses emerging from the cell: <a href="https://doi.org/10.1016/0042-6822(73)90432-7">phage P2 and phage P4</a>.</p>
<p>Bacteriophage P4 is a temperate virus, meaning it can integrate into the chromosome of its host cell and lie dormant. When P2 infects a cell already harboring P4, the latent P4 quickly wakes up and <a href="https://doi.org/10.1128/mr.57.3.683-702.1993">uses the genetic instructions of P2</a> to make hundreds of its own small viral particles. The unsuspecting P2 is lucky to replicate a few times, if at all. In this case, biologists refer to P2 as a “helper” virus, because the satellite P4 needs P2’s genetic material to replicate and spread. </p>
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<figcaption><span class="caption">Bacteriophages are viruses that infect bacteria.</span></figcaption>
</figure>
<p>Subsequent research has shown that most bacterial species have a <a href="https://doi.org/10.1038/s41396-018-0156-3">diverse set of satellite-helper systems</a>, like that of P4-P2. But viral satellites are not limited to bacteria. Shortly after the largest known virus, mimivirus, was discovered in 2003, scientists also found its <a href="https://doi.org/10.1038/nature07218">satellite, which they named Sputnik</a>. <a href="https://doi.org/10.1016/0042-6822(81)90531-6">Plant viral satellites</a> that lurk in plant cells waiting for other viruses are also widespread and can have <a href="https://doi.org/10.1007/s11262-020-01806-9">important effects on crops</a>.</p>
<h2>Viral arms race</h2>
<p>Although researchers have found satellite-helper viral systems in pretty much <a href="https://doi.org/10.1016/j.coviro.2018.08.002">every domain of life</a>, their importance to biology remains underappreciated. Most obviously, viral satellites have a direct impact on their “helper” viruses, typically maiming them but <a href="https://doi.org/10.1016/j.coviro.2018.08.002">sometimes making them more efficient killers</a>. Yet that is probably the least of their contributions to biology. </p>
<p>Satellites and their helpers are also engaged in an <a href="https://doi.org/10.1371/journal.pgen.1005609">endless evolutionary arms race</a>. Satellites evolve new ways to exploit helpers and helpers evolve countermeasures to block them. Because both sides are viruses, the results of this internecine war necessarily include something of interest to people: antivirals.</p>
<p>Recent work indicates that many antiviral systems thought to have evolved in bacteria, like the CRISPR-Cas9 molecular scissors used in gene editing, may have <a href="https://doi.org/10.1093/nar/gkac845">originated in phages and their satellites</a>. Somewhat ironically, with their high turnover and mutation rates, helper viruses and their satellites turn out to be <a href="https://doi.org/10.1016/j.chom.2022.02.018">evolutionary hot spots for antiviral weaponry</a>. Trying to outsmart each other, satellite and helper viruses have come up with an unparalleled array of antiviral systems for researchers to exploit.</p>
<h2>MindFlayer and MiniFlayer</h2>
<p>Viral satellites have the potential to transform how researchers understand antiviral strategies, but there is still a lot to learn about them. In our recent work, my collaborators and I describe a satellite bacteriophage completely unlike previously known satellites, one that has evolved a <a href="https://doi.org/10.1038/s41396-023-01548-0">unique, spooky lifestyle</a>. </p>
<p><a href="https://phages.umbc.edu/">Undergraduate phage hunters</a> at the University of Maryland, Baltimore County isolated a <a href="https://phagesdb.org/phages/MiniFlayer/">satellite phage called MiniFlayer</a> from the soil bacterium <em>Streptomyces scabiei</em>. MiniFlayer was found in close association with a helper virus called <a href="https://phagesdb.org/phages/MindFlayer/">bacteriophage MindFlayer</a> that infects the <em>Streptomyces</em> bacterium. But further research revealed that MiniFlayer was no ordinary satellite.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C1084%2C1097&q=45&auto=format&w=1000&fit=clip"><img alt="Microscopy image of a small round virus colored violet attached to the base of a larger round virus colored gray with a long tail" src="https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C1084%2C1097&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=607&fit=crop&dpr=1 600w, https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=607&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=607&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=763&fit=crop&dpr=1 754w, https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=763&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/557149/original/file-20231101-28-nu795n.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=763&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">This image shows <em>Streptomyces</em> satellite phage MiniFlayer (purple) attached to the neck of its helper virus, <em>Streptomyces</em> phage MindFlayer (gray).</span>
<span class="attribution"><a class="source" href="https://doi.org/10.1038/s41396-023-01548-0">Tagide deCarvalho</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
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<p>MiniFlayer is the first satellite phage known to have lost its ability to lie dormant. Not being able to lie in wait for your helper to enter the cell poses an important challenge to a satellite phage. If you need another virus to replicate, how do you guarantee that it makes it into the cell around the same time you do? </p>
<p>MiniFlayer addressed this challenge with evolutionary aplomb and horror-movie creativity. Instead of lying in wait, MiniFlayer has gone on the offensive. Borrowing from both “Dracula” and “Alien,” this satellite phage <a href="https://doi.org/10.1038/s41396-023-01548-0">evolved a short appendage</a> that allows it to latch onto its helper’s neck like a vampire. Together, the unwary helper and its passenger travel in search of a new host, where the viral drama will unfold again. We don’t yet know how MiniFlayer subdues its helper, or whether MindFlayer has evolved countermeasures.</p>
<p>If the recent pandemic has taught us anything, it is that our <a href="https://doi.org/10.1007/s00018-022-04635-1">supply of antivirals is rather limited</a>. Research on the complex, intertwined and at times predatory nature of viruses and their satellites, like the ability of MiniFlayer to attach to its helper’s neck, has the potential to open new avenues for antiviral therapy.</p><img src="https://counter.theconversation.com/content/216344/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ivan Erill receives funding from the US National Science Foundation. He is affiliated with the Universitat Autònoma de Barcelona. </span></em></p>Researchers discovered a satellite virus latching onto the neck of another virus called MindFlayer. Studying the viral arms race between similar viruses could lead to new ways to fight infections.Ivan Erill, Professor of Biological Sciences, University of Maryland, Baltimore CountyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2104572023-08-29T02:25:36Z2023-08-29T02:25:36ZI think I have the flu. Should I ask my GP for antivirals?<figure><img src="https://images.theconversation.com/files/544456/original/file-20230824-29-51fiyz.jpg?ixlib=rb-1.1.0&rect=613%2C0%2C5497%2C4086&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.pexels.com/photo/woman-lying-on-bed-while-blowing-her-nose-3807629/">Andrea Piacquadio/Pexels</a></span></figcaption></figure><p>If you test positive for COVID and you’re eligible for antivirals, you’ll likely ask your GP for a script to protect you from severe disease. </p>
<p><a href="https://healthdispatch.com.au/news/immunisation-coalition-urging-people-with-flu-like-symptoms-to-g">Antivirals</a> are also available to fight influenza viruses, via a doctor’s prescription. But they have a mixed history, with their benefits at times <a href="https://theconversation.com/controversies-in-medicine-the-rise-and-fall-of-the-challenge-to-tamiflu-38287">overstated</a>. </p>
<p>It can be difficult to get an appointment to see your GP. So when should you make the effort to see a GP for a prescription for influenza antivirals? And how effective are they?</p>
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Read more:
<a href="https://theconversation.com/controversies-in-medicine-the-rise-and-fall-of-the-challenge-to-tamiflu-38287">Controversies in medicine: the rise and fall of the challenge to Tamiflu</a>
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<h2>What exactly is influenza?</h2>
<p>The flu is primarily a viral infection of the respiratory system that can spread through sneezing, coughing, or touching contaminated objects then touching your nose or mouth. </p>
<p>Common symptoms include headache, sore throat, fever, runny or blocked nose and body aches that last a week or more.</p>
<p>Influenza is actually a group of viruses, divided into several <a href="https://www.cdc.gov/flu/about/viruses/types.htm#:%7E:text=There%20are%20four%20types%20of,global%20epidemics%20of%20flu%20disease,%20https://www.cdc.gov/flu/professionals/acip/background-epidemiology.htm">sub-groups</a>. Flu A and B are the <a href="https://www.health.gov.au/resources/collections/aisr?language=en,%20https://www.health.gov.au/resources/collections/australian-influenza-surveillance-reports-2023?language=en">most common groups</a> that circulate in humans. </p>
<h2>What are flu antivirals?</h2>
<p>Influenza antivirals, target specific parts of the viral life cycle, which prevents the virus replicating and spreading. </p>
<p>Most flu antivirals <a href="https://www.nejm.org/doi/full/10.1056/NEJMra050740">target</a> neuraminidase, an important enzyme the virus uses to release itself from cells.</p>
<p>On the other hand, COVID antivirals work by inhibiting other parts of the viral life cycle involved in the <a href="https://www.tga.gov.au/news/media-releases/tga-provisionally-approves-two-oral-covid-19-treatments-molnupiravir-lagevrio-and-nirmatrelvir-ritonavir-paxlovid">virus replicating itself</a>.</p>
<p>Three influenza antivirals are <a href="https://australianprescriber.tg.org.au/articles/influenza-overview-on-prevention-and-therapy.html#r20">used in Australia</a>. Relenza (zanamivir) is an inhaled powder and Tamiflu (oseltamivir) is a capsule; both are five-day treatments. Rapivab (peramivir) is a single injection. </p>
<p>These antivirals may also come with <a href="https://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm">side effects</a>, such as a headache, vomiting, cough, or <a href="https://www.immunisationcoalition.org.au/resources/antiviral-treatments-for-influenza/">fever</a>.</p>
<p>Tamiflu and Relenza generally cost A$40-50 in Australia, plus the cost of the consultation fee with your doctor, if applicable. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/should-i-get-a-flu-vaccine-this-year-heres-what-you-need-to-know-203406">Should I get a flu vaccine this year? Here's what you need to know</a>
</strong>
</em>
</p>
<hr>
<h2>How effective are antivirals for the flu?</h2>
<p>Antivirals have the greatest effect if started 24-72 hours after symptoms. This is to prevent the virus from reaching <a href="https://www.mdpi.com/1660-4601/19/5/3018">high levels in the body</a>.</p>
<p>Among healthy adults, if Relenza or Tamiflu are started within 48 hours from your first symptoms, they can <a href="https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD008965.pub4/full">reduce the duration</a> of symptoms such as cough, blocked nose, sore throat, fatigue, headache, muscle pain and fever by just under a day. </p>
<p>For people who have developed severe flu symptoms or who have existing health conditions such as heart disease or chronic obstructive pulmonary disease (COPD), antivirals that start later (but still before day five of symptoms) can still reduce the <a href="https://academic.oup.com/cid/article/52/4/457/378776?login=true">severity of infection</a> and reduce the <a href="https://thorax.bmj.com/content/thoraxjnl/65/6/510.full.pdf?frbrVersion=3">chance of</a> <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/215903">hospitalisation</a> and <a href="https://academic.oup.com/jac/article/72/11/2990/4091484?login=false">death</a>.</p>
<figure class="align-center ">
<img alt="Older man coughs, while his partner looks concerned" src="https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544481/original/file-20230824-17-g9r2zk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Antivirals need to be started early.</span>
<span class="attribution"><a class="source" href="https://www.pexels.com/photo/man-in-gray-sweater-sitting-beside-woman-5790716/">Vlada Karpovich/Pexels</a></span>
</figcaption>
</figure>
<p>In a study from the 2009 swine flu (H1N1) pandemic in the United States, treatment with antivirals (Tamiflu and Relenza) <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358088/">reduced</a> the chance of needing to be hospitalised. Around 60% of hospitalisations prevented were among 18-64 years olds, around 20% in children 0-17 years, and 20% in adults aged over 65.</p>
<p>The research is less clear about whether antivirals prevent the development of flu complications such as secondary bacterial pneumonia. They might, but so far the data aren’t clear.</p>
<h2>Are flu antivirals becoming less effective?</h2>
<p>Antiviral resistance to Tamiflu has been <a href="https://link.springer.com/article/10.1007/s10096-020-03840-9">reported</a> around the world, mostly in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7223162/">immunocompromised people</a>, as they <a href="https://link.springer.com/article/10.1007/s10096-020-03840-9">have</a> a weakened immune system that allows higher viral loads and prolonged viral shedding.</p>
<p>The impact of the antiviral resistance is unclear but there is evidence indicating resistant strains can uphold their ability to replicate effectively and spread. So far it’s not clear if these stains cause more severe disease.</p>
<p>However, government agencies and surveillance programs are constantly monitoring the spread of antiviral resistance. Currently there is <a href="https://www.cdc.gov/flu/treatment/antiviralresistance.htm">minimal concern</a> for strains that are resistant to Tamiflu or Relenza.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-are-there-so-many-drugs-to-kill-bacteria-but-so-few-to-tackle-viruses-137480">Why are there so many drugs to kill bacteria, but so few to tackle viruses?</a>
</strong>
</em>
</p>
<hr>
<h2>Antivirals can also prevent the flu if you’ve been exposed</h2>
<p>Tamiflu and Relenza can also be used to <a href="https://onlinelibrary.wiley.com/doi/10.1111/irv.12046">prevent flu infections</a>, if we’re exposed to the virus or come into contact with infected people.</p>
<p>Some studies suggest Tamiflu and Relenza can <a href="https://www.bmj.com/content/326/7401/1235.long">reduce the chance of developing symptomatic influenza</a> by 70-90%.</p>
<p>Many health agencies around the world <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8165743/">recommend</a> “prophylactic” treatment for high-risk patients in hospitals or age care setting when people have been in contact with others infected with influenza. </p>
<figure class="align-center ">
<img alt="Woman at supermarket reaches for an orange" src="https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544484/original/file-20230824-8994-y4fyo6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Antivirals can stop people who have been exposed to influenza from developing severe illness.</span>
<span class="attribution"><a class="source" href="https://www.pexels.com/photo/woman-wearing-mask-in-supermarket-3962289/">Anna Shvets/Pexels</a></span>
</figcaption>
</figure>
<h2>So who should talk to their GP about a prescription?</h2>
<p><a href="https://www.health.nsw.gov.au/Infectious/factsheets/Pages/racf-antiviral-treatments-and-prophylaxis.aspx#:%7E:text=The%20Australian%20Therapeutic%20Guidelines*%20recommends,of%20severe%20disease%20from%20influenza.&text=people%20with%20chronic%20conditions%20including,heart%20disease">Australian guidelines recommend</a> doctors offer antivirals to people with influenza who have severe disease or complications. </p>
<p>Doctors can also consider treatment for people at higher risk of developing severe disease from influenza. This includes:</p>
<ul>
<li>adults aged 65 years or older</li>
<li>pregnant women</li>
<li>people with certain chronic conditions (heart disease, Down syndrome, obesity, chronic respiratory conditions, severe neurological conditions)</li>
<li>people with compromised immunity</li>
<li>Aboriginal and Torres Strait Islander people</li>
<li>children aged five years or younger</li>
<li>residents of long-term residential facilities</li>
<li>homeless people.</li>
</ul>
<p>Doctors can prescribe antivirals for the prevention of influenza <a href="https://australianprescriber.tg.org.au/articles/influenza-overview-on-prevention-and-therapy.html#r20">in</a> vulnerable people who have been exposed to the virus.</p>
<p>Antiviral treatment also can be <a href="https://www.cdc.gov/flu/professionals/antivirals/summary-clinicians.htm#:%7E:text=Antiviral%20treatment%20also%20can%20be,48%20hours%20of%20illness%20onset">considered</a> for otherwise healthy symptomatic patients who have confirmed or suspected influenza, if they can start treatment within 48 hours of developing symptoms.</p>
<p>In some instances a doctors can make a clinical diagnosis of influenza based on the symptoms and known close flu positive contacts of the patient. However, it is preferred to have flu diagnosed by one of the approved diagnostic tests, such as a <a href="https://24-7medcare.com.au/influenza/australian-gp-influenza-2023-guide/">rapid antigen test</a> (RAT) or the more accurate <a href="https://www.health.nsw.gov.au/Infectious/factsheets/Pages/influenza_factsheet.aspx">PCR test</a>, similar to what is perfomed for COVID. There are also now combo tests that can <a href="https://www.tga.gov.au/news/media-releases/first-combination-covid-19-and-influenza-self-tests-approved-australia">distinguish between SARS-CoV-2 and influenza virus</a>.</p>
<p>Remember, the flu can cause <a href="https://www.abc.net.au/news/2023-07-23/flu-season-hitting-children-hard-antivirals-may-help/102633722">severe illness or death</a>, particularly among people from the high-risk groups. So if you think you might have the flu, wear a mask and stay away to avoid spreading the virus to others. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/what-happens-in-our-body-when-we-encounter-and-fight-off-a-virus-like-the-flu-sars-cov-2-or-rsv-207023">What happens in our body when we encounter and fight off a virus like the flu, SARS-CoV-2 or RSV?</a>
</strong>
</em>
</p>
<hr>
<img src="https://counter.theconversation.com/content/210457/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lara Herrero receives funding from NHMRC. </span></em></p><p class="fine-print"><em><span>Wesley Freppel and Yong Qian Koo do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>It can be difficult to an appointment to see your GP. So when should you make the effort to see a GP for a prescription for influenza antivirals? And how effective are they?Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityWesley Freppel, Research Fellow, Institute for Glycomics, Griffith UniversityYong Qian Koo, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2050252023-06-08T20:07:07Z2023-06-08T20:07:07ZLong COVID could be caused by the virus lingering in the body. Here’s what the science says<figure><img src="https://images.theconversation.com/files/530286/original/file-20230606-29-9qrejq.jpg?ixlib=rb-1.1.0&rect=58%2C226%2C5540%2C3505&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://unsplash.com/photos/cfKO58M1QpY">Alexander Grey/Unsplash</a></span></figcaption></figure><p>While most people survive and recover from COVID, for some people symptoms can <a href="https://www.nature.com/articles/s41586-021-03553-9">persist for months</a> or years. When symptoms last longer than 12 weeks, the condition is known as <a href="https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html">long COVID</a>. </p>
<p>Long COVID encompasses up to <a href="https://www.nature.com/articles/s41579-022-00846-2?utm_source=substack&utm_medium=email">200 different symptoms</a>. To determine evidence-based treatments for these symptoms, we need to understand the causes. One factor that may be associated with long COVID is that the virus hasn’t fully cleared from the body after the initial infection. </p>
<p>We know from other viruses that viral fragments can remain in different tissues for months or even years. This could be the case with SARS-CoV-2, the virus that causes COVID. Here’s what the science says so far. </p>
<h2>Other viruses lurk in the body</h2>
<p>Herpesviruses (such as Epstein-Barr virus, the cause of glandular fever), as well as HIV (human immunodeficiency virus) can exist in a “latency state” for life. This means the virus conceals itself within cells and remains dormant. </p>
<p>HIV, in particular, can remain dormant in infected cells throughout the body. Even though it’s inactive, it can still promote immune activation and inflammation. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/hiv-latency-a-high-stakes-game-of-hide-and-seek-49665">HIV latency: a high-stakes game of hide and seek</a>
</strong>
</em>
</p>
<hr>
<p>Other viruses such as <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7728251/">Zika</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492426/">measles</a> and <a href="https://bmjopen.bmj.com/content/6/1/e008859">Ebola</a> have been found in tissues of infected people months or years after initial infection. This viral persistence can <a href="https://www.ahajournals.org/doi/10.1161/circulationaha.105.548156">cause chronic illness</a>.</p>
<p>Several studies have shown COVID can also reactivate the Epstein-Barr virus, which has remained in the body in a latent state. Research shows this has been <a href="https://www.jci.org/articles/view/163669">linked to</a> fatigue and problems with thinking and reasoning in <a href="https://www.mdpi.com/2076-0817/10/6/763">people with long COVID</a>. </p>
<figure class="align-center ">
<img alt="Man looks at laptop, confused" src="https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Latent viruses can cause fatigue and problems with thinking and reasoning.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/4-EeTnaC1S4">Wes Hicks/Unsplash</a></span>
</figcaption>
</figure>
<h2>How do we know COVID stays in the body?</h2>
<p>Several studies have identified the genetic sequences of SARS-CoV-2 (RNA) as well as SARS-CoV-2 proteins in tissues and stool (poo) samples months following infection. </p>
<p>These studies include multiple autopsy reports that <a href="https://www.nature.com/articles/s41586-022-05542-y">found viral RNA and protein in a variety of tissues</a> from people who died up to seven months after infection. SARS-CoV-2 RNA was detected in at least half the samples of heart, lymph glands, eye, nerve, brain and lung tissue tested. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/long-covid-puts-some-people-at-higher-risk-of-heart-disease-they-need-better-long-term-monitoring-202596">Long COVID puts some people at higher risk of heart disease -- they need better long-term monitoring</a>
</strong>
</em>
</p>
<hr>
<p>In people who survived, <a href="https://www.nature.com/articles/s41586-021-03207-w">viral RNA was found</a> four months after infection within intestinal tissues obtained through colonoscopy, when a thin tube is used to take tissue from the large intestine. These patients had asymptomatic COVID and were PCR-negative from swabs of the nose and throat at four months.</p>
<p>A 2022 study found SARS-CoV-2 in the stool of about half of the participants in the first week after infection. At four months, there was no virus present in the respiratory tract but <a href="https://doi.org/10.1016/j.medj.2022.04.001">12.7% of stool samples were RNA positive</a>. A further 3.8% of faecal samples remained positive for RNA at seven months. </p>
<p><a href="https://doi.org/10.1016/S2213-2600(21)00240-X">Initial studies</a> did not always suggest a strong relationship between the long-term detection of SARS-CoV-2 and long COVID symptoms.</p>
<p>But more recently, the presence of SARS-CoV-2 RNA (or protein translated from RNA) in the <a href="https://academic.oup.com/cid/article/76/3/e487/6686531">blood</a> and gut tissue was found to <a href="https://doi.org/10.1053/j.gastro.2022.04.037">increase the likelihood</a> of developing long COVID symptoms.</p>
<figure class="align-center ">
<img alt="Person gets a blood test" src="https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=335&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=335&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=335&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=421&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=421&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=421&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The presence of SARS-CoV-2 in the blood increases the likelihood of developing long COVID symptoms.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/ufwC2cmbaaI">Nguyễn Hiệp/Unsplash</a></span>
</figcaption>
</figure>
<h2>How might the delay in clearing the virus impact people with long COVID?</h2>
<p>Delayed clearance of SARS-CoV-2 particles in different parts of the body could drive illness through several potential processes:</p>
<p><strong>1) Inflammation</strong>. The continued immune stimulation by viral proteins causes inflammation, makes our immune system tired, and alters how our immune cells work as time goes on. </p>
<p><a href="https://www.nature.com/articles/s41590-021-01113-x">We have previously shown</a> immune dysfunction and inflammation persist up to eight months in people with long COVID that initially had mild to moderate disease. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/when-does-covid-become-long-covid-and-whats-happening-in-the-body-when-symptoms-persist-heres-what-weve-learnt-so-far-188976">When does COVID become long COVID? And what's happening in the body when symptoms persist? Here's what we've learnt so far</a>
</strong>
</em>
</p>
<hr>
<p><strong>2) Activation of other dormant viruses</strong>. The continued immune response to persistent SARS-CoV-2 can cause reactivation of latent viruses. </p>
<p>Antibodies reactive to Epstein-Barr virus are elevated in people with long COVID suggesting Epstein-Barr virus <a href="https://doi.org/10.1101/2022.08.09.22278592">reactivation</a>, likely through activating the immune system.</p>
<p>Other latent viruses, such as human endogenous retroviruses (HERVs; ancient viruses that have become a part of our DNA, like a genetic fossil) have recently been shown to become reactivated after infection. HERV proteins <a href="https://www.sciencedirect.com/science/article/pii/S2589004223006818">were detected</a> in blood cells and tissues of COVID patients. </p>
<p>These proteins could potentially drive inflammatory processes in long COVID.</p>
<figure class="align-center ">
<img alt="3D illustration of the Epstein-Barr virus in green and red" src="https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Reactivation of the Epstein-Barr virus could drive inflammation in long COVID.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/epsteinbarr-virus-ebv-herpes-which-causes-556379407">Shutterstock</a></span>
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<p><strong>3) Antibodies made by combating SARS-CoV-2 could become “self” reactive.</strong> These autoantibodies (antibodies produced by our immune system that mistakenly target and attack our own body’s tissues or organs) might cross-react with host receptors or proteins and <a href="https://www.nature.com/articles/s41577-020-00458-y">drive autoimmune</a> disease. </p>
<p>Importantly, recent studies have shown new onset of autoimmune diseases (such as type 1 diabetes, inflammatory bowel disease and psoriasis) are significantly associated with SARS-CoV-2 infection and <a href="https://www.nature.com/articles/s41584-023-00964-y">a link between autoimmunity and long COVID</a> is plausible. </p>
<p>This suggests COVID not only has immediate health impacts but could also potentially trigger long-term changes in the immune system.</p>
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<strong>
Read more:
<a href="https://theconversation.com/viral-infections-including-covid-are-among-the-important-causes-of-dementia-one-more-reason-to-consider-vaccination-190962">Viral infections including COVID are among the important causes of dementia – one more reason to consider vaccination</a>
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<p>While the studies mentioned above provide initial evidence of persistence of SARS-CoV-2 long after initial infection, more studies are needed to show a convincing link between lingering virus and long COVID. This should include examination of viral RNA and protein in both blood and tissues in people with long COVID independent of disease severity. And it must involve well-developed cohort studies that track large groups of people internationally.</p>
<p><a href="https://clinicaltrials.gov/ct2/show/NCT05668091">Several</a> <a href="https://clinicaltrials.gov/ct2/show/NCT05576662">trials are underway</a> to assess whether treating long COVID with antivirals such as Paxlovid may reduce viral antigens and improve symptoms, although this remains experimental.</p><img src="https://counter.theconversation.com/content/205025/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Stephen Kent receives funding from the NHMRC, the MRFF, the ARC and the NIH. </span></em></p><p class="fine-print"><em><span>Chan Phetsouphanh receives funding from NHMRC and MRFF. </span></em></p>We know from other viruses that viral fragments can remain in different tissues for months or even years. This could be the case for long COVID.Stephen Kent, Professor and Laboratory Head, The University of MelbourneChansavath Phetsouphanh, Senior Research Associate, Kirby Institute, UNSW SydneyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2020842023-05-08T12:18:30Z2023-05-08T12:18:30ZGain-of-function research is more than just tweaking risky viruses – it’s a routine and essential tool in all biology research<figure><img src="https://images.theconversation.com/files/523909/original/file-20230502-4095-u8oni1.jpg?ixlib=rb-1.1.0&rect=0%2C94%2C1500%2C1221&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Gain-of-function experiments in the lab can help researchers get ahead of viruses naturally gaining the ability to infect people in the wild.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/molecule-illustration-royalty-free-illustration/1423893041">KTSDesign/Science Photo Library via Getty Images</a></span></figcaption></figure><p>The term “gain of function” is often taken to refer to research with viruses that puts society at risk of an infectious disease outbreak for questionable gain. Some research on emerging viruses can result in variants that gain the ability to infect people but this does not necessarily mean the research is dangerous or that it is not fruitful. Concerns have focused on lab research on the <a href="https://www.theguardian.com/world/2012/mar/28/bird-flu-mutant-strains">virus that causes bird flu</a> in 2012 and on the <a href="https://theconversation.com/why-gain-of-function-research-matters-162493">virus that causes COVID-19</a> since 2020. The National Institutes of Health had previously implemented a <a href="https://www.science.org/content/article/nih-lifts-3-year-ban-funding-risky-virus-studies">three-year moratorium</a> on gain-of-function research on certain viruses, and some U.S. legislatures have <a href="https://www.washingtonexaminer.com/news/senate/texas-state-ban-gain-function-research-covid-pandemic">proposed bills prohibiting</a> gain-of-function research on “potentially pandemic pathogens.”</p>
<p>The possibility that a genetically modified virus could escape the lab needs to be taken seriously. But it does not mean that gain-of-function experiments are inherently risky or the purview of mad scientists. In fact, gain-of-function approaches are a fundamental tool in biology used to study much more than just viruses, contributing to many, if not most, modern discoveries in the field, including <a href="https://doi.org/10.3201%2Feid2305.161556">penicillin</a>, <a href="https://theconversation.com/anti-cancer-car-t-therapy-reengineers-t-cells-to-kill-tumors-and-researchers-are-expanding-the-limited-types-of-cancer-it-can-target-196471">cancer immunotherapies</a> and <a href="https://www.sciencedaily.com/releases/2015/02/150204134119.htm">drought-resistant crops</a>.</p>
<p>As <a href="https://scholar.google.com/citations?user=IXDoiY4AAAAJ&hl=en">scientists who</a> <a href="https://scholar.google.com/citations?user=GBQiazwAAAAJ&hl=en">study viruses</a>, we believe that misunderstanding the term “gain of function” as something nefarious comes at the cost of progress in human health, ecological sustainability and technological advancement. Clarifying what gain-of-function research really is can help clarify why it is an essential scientific tool.</p>
<h2>What is gain of function?</h2>
<p>To study how a living thing operates, scientists can change a specific part of it and then observe the effects. These changes sometimes result in the organism’s gaining a function it didn’t have before or losing a function it once had. </p>
<p>For example, if the goal is to enhance the tumor-killing ability of immune cells, researchers can take a sample of a person’s immune cells and modify them to express a protein that specifically targets cancer cells. This mutated immune cell, called a <a href="https://theconversation.com/anti-cancer-car-t-therapy-reengineers-t-cells-to-kill-tumors-and-researchers-are-expanding-the-limited-types-of-cancer-it-can-target-196471">CAR-T cell</a> thereby “gains the function” of being able to bind to cancerous cells and kill them. The advance of similar immunotherapies that help the immune system attack cancer cells is based on the exploratory research of scientists who synthesized such “<a href="https://doi.org/10.1007/BF00820662">Frankenstein” proteins</a> in the 1980s. At that time, there was no way to know how useful these chimeric proteins would be to cancer treatment today, some 40 years later. </p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/mXADrg_ckhI?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">CAR-T cell therapy involves giving a patient’s immune cells an increased ability to target cancer cells.</span></figcaption>
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<p>Similarly, by adding specific genes into rice, corn or wheat plants that increase their production in diverse climates, scientists have been able to produce plants that are able to grow and thrive in geographical regions they previously could not. This is a critical advance to maintain food supplies in the face of climate change. Well-known examples of food sources that have their origins in gain-of-function research <a href="https://www.sciencenews.org/article/rice-agriculture-feeds-world-climate-change-drought-flood-risk">include rice plants</a> that can grow in high flood plains or in drought conditions or that contain vitamin A to reduce malnutrition.</p>
<h2>Medical advances from gain-of-function research</h2>
<p>Gain-of-function experiments are ingrained in the scientific process. In many instances, the benefits that stem from gain-of-function experiments are not immediately clear. Only decades later does the research bring a new treatment to the clinic or a new technology within reach. </p>
<p>The development of most antibiotics have relied on the <a href="https://doi.org/10.3389/fcimb.2021.684515">manipulation of bacteria or mold</a> in gain-of-function experiments. Alexander Fleming’s initial discovery that the mold <em>Penicillium rubens</em> could produce a compound toxic to bacteria was a profound medical advance. But it wasn’t until scientists experimented with <a href="https://www.sciencemuseum.org.uk/objects-and-stories/how-was-penicillin-developed">growth conditions and mold strains</a> that therapeutic use of penicillin became feasible. Using a specific growth medium allowed the mold to gain the function of increased penicillin production, which was essential for its mass production and widespread use as a drug. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Worker monitoring penicillin capsules coming down production line" src="https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=759&fit=crop&dpr=1 600w, https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=759&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=759&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=954&fit=crop&dpr=1 754w, https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=954&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/523678/original/file-20230501-1518-hmu9o0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=954&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Gain-of-function research played a key role in the development and mass production of penicillin.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/penicillin-capsules-being-checked-as-they-come-off-the-news-photo/2667016">Wesley/Stringer/Hulton Archive via Getty Images</a></span>
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<p>Research on <a href="https://doi.org/10.1128%2FAAC.02381-18">antibiotic resistance</a> also relies heavily on gain-of-function approaches. Studying how bacteria <a href="https://theconversation.com/looming-behind-antibiotic-resistance-is-another-bacterial-threat-antibiotic-tolerance-200226">gain resistance</a> against drugs is essential to developing new treatments microbes are unable to evade quickly.</p>
<p>Gain-of-function research in virology has also been critical to the advancement of science and health. <a href="https://www.cancer.gov/news-events/cancer-currents-blog/2018/oncolytic-viruses-to-treat-cancer">Oncolytic viruses</a> are genetically modified in the laboratory to infect and kill cancerous cells like melanoma. Similarly, the <a href="https://www.cdc.gov/coronavirus/2019-ncov/vaccines/different-vaccines/overview-COVID-19-vaccines.html">Johnson & Johnson COVID-19 vaccine</a> contains an adenovirus altered to produce the spike protein that helps the COVID-19 virus infect cells. Scientists developed <a href="https://onlinelibrary.wiley.com/doi/10.1002/(SICI)1099-1654(199910/12)9:4%3C237::AID-RMV252%3E3.0.CO;2-G">live attenuated flu vaccines</a> by adapting them to grow at low temperatures and thereby lose the ability to grow at human lung temperatures. </p>
<p>By giving viruses new functions, scientists were able to develop new tools to treat and prevent disease.</p>
<h2>Nature’s gain-of-function experiments</h2>
<p>Gain-of-function approaches are needed to advance understanding of viruses in part because these processes already occur in nature.</p>
<p>Many viruses that infect such nonhuman animals as bats, pigs, birds and mice have the potential to <a href="https://theconversation.com/what-is-spillover-bird-flu-outbreak-underscores-need-for-early-detection-to-prevent-the-next-big-pandemic-200494">spill over into people</a>. Every time a virus copies its genome, it makes mistakes. Most of these mutations are detrimental – they reduce a virus’s ability to replicate – but some may allow a virus to replicate faster or better in human cells. Variant viruses with these rare, beneficial mutations will spread better than other variants and therefore come to dominate the viral population – that is <a href="https://www.amnh.org/exhibitions/darwin/evolution-today/natural-selection-vista">how natural selection works</a>.</p>
<p>If these viruses can replicate even a little bit within people, they have the potential to adapt and thereby thrive in their new human hosts. That is nature’s gain-of-function experiment, and <a href="https://doi.org/10.1093/ve/veaa016">it is</a> <a href="https://doi.org/10.1016/j.chom.2020.08.011">happening constantly</a>.</p>
<p>Gain-of-function experiments in the lab can help scientists <a href="https://doi.org/10.1126%2Fscience.1222526">anticipate the changes</a> viruses may undergo in nature by understanding what specific features allow them to transmit between people and infect them. In contrast to nature’s experiments, these are conducted in <a href="https://www.cdc.gov/labs/BMBL.html">highly controlled lab conditions</a> designed to limit infection risk to laboratory personnel and others, including air flow control, personal protective equipment and waste sterilization.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="People in protective clothing collecting dead pelicans on a beach" src="https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/523674/original/file-20230501-20-lxf4la.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Researchers and public health officials are concerned that the bird flu virus is evolving to more readily infect people.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/BirdFluMutations/6895d38a33de468c93c14da427b4dfff">Guadalupe Pardo/AP Photo</a></span>
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</figure>
<p>It is important that researchers carefully observe lab safety to minimize the theoretical risk of infecting the general population. It is equally important that virologists continue to apply the tools of modern science to gauge the risk of natural viral spillovers before they become outbreaks. </p>
<p>A <a href="https://theconversation.com/as-bird-flu-continues-to-spread-in-the-us-and-worldwide-whats-the-risk-that-it-could-start-a-human-pandemic-4-questions-answered-200204">bird flu outbreak</a> is currently raging across multiple continents. While the H5N1 virus is primarily infecting birds, some people have gotten sick too. More spillover events can change the virus in ways that would allow it to <a href="https://doi.org/10.1126/science.adi1013">transmit more efficiently among people</a>, potentially leading to a pandemic. </p>
<p>Scientists have a better appreciation of the tangible risk of bird flu spillover because of <a href="https://doi.org/10.1126/science.1213362">gain-of-function experiments</a> <a href="https://doi.org/10.1038/nature10831">published a decade ago</a>. Those lab studies showed that bird flu viruses could be transmitted through the air between ferrets within a few feet of one another. They also revealed multiple features of the evolutionary path the H5N1 virus would need to take before it becomes transmissible in mammals, informing what signatures researchers need to look out for during surveillance of the current outbreak.</p>
<h2>Oversight on gain of function</h2>
<p>Perhaps this sounds like a semantic argument, and in many respects it is. <a href="https://www.statnews.com/2021/12/23/gain-of-function-research-advances-knowledge-and-saves-lives/">Many researchers</a> would likely agree that gain of function as a general tool is an important way to study biology that should not be restricted, while also arguing that it should be curtailed for research on specific dangerous pathogens. The problem with this argument is that pathogen research needs to include gain-of-function approaches in order to be effective – just as in any area of biology.</p>
<p><a href="https://doi.org/10.1128/jvi.00089-23">Oversight of gain-of-function research</a> on potential pandemic pathogens already exists. Multiple layers of safety measures at the institutional and national levels minimize the risks of virus research.</p>
<p>While updates to current oversight are not unreasonable, we believe that <a href="https://www.nih.gov/about-nih/who-we-are/nih-director/statements/statement-report-national-science-advisory-board-biosecurity">blanket bans or additional restrictions</a> on gain-of-function research do not make society safer. They may instead slow research in areas ranging from cancer therapies to agriculture. Clarifying which specific research areas are of concern regarding gain-of-function approaches can help identify how the current oversight framework can be improved.</p><img src="https://counter.theconversation.com/content/202084/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Seema Lakdawala receives funding from National Institutes of Health and the Flu Lab. </span></em></p><p class="fine-print"><em><span>Anice Lowen receives research funding from the National Institutes of Health and Flu Lab. </span></em></p>From cancer immunotherapy and antibiotics to GMO crops and pandemic surveillance, gain of function is a cornerstone of basic research.Seema Lakdawala, Associate Professor of Microbiology and Immunology at Emory University and Adjunct Professor Microbiology and Molecular Genetics, University of PittsburghAnice Lowen, Associate Professor of Microbiology and Immunology, Emory UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1946272022-12-20T13:37:59Z2022-12-20T13:37:59ZChickenpox and shingles virus lying dormant in your neurons can reactivate and increase your risk of stroke – new research identified a potential culprit<figure><img src="https://images.theconversation.com/files/501603/original/file-20221216-16-hwr4sm.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C3264%2C2448&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Cells secrete exosomes carrying molecules that play a critical role in both health and disease.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/cells-secreting-exosomes-royalty-free-image/1174299609">Meletios Verras/iStock via Getty Images Plus</a></span></figcaption></figure><p><a href="https://doi.org/10.1038/s41467-018-03569-2">Over 90% of the world population</a> has the virus that causes chickenpox lying dormant in their nervous system. Most people contract the varicella zoster virus, or VZV, when they get chickenpox as children. For around a third of these people, this same virus will reactivate years later and cause shingles, also called herpes zoster.</p>
<p>While most people are familiar with the painful rash that VZV causes for shingles, a wide spectrum of other complications can also occur even without visible skin symptoms. Among the most severe is stroke, in particular ischemic stroke, which occurs when the blood supply to the brain is restricted by narrowing arteries or blocked by a clot. </p>
<p>People with shingles have an approximately <a href="https://doi.org/10.1093/infdis/jiac405">80% higher risk of stroke</a> than those without the disease, and this risk stays elevated for up to a year after the rash has resolved. Stroke risk is nearly doubled for those with the rash on their face, and tripled for those <a href="https://doi.org/10.1212/WNL.0000000000000038">under the age of 40</a>.</p>
<p>The mechanism behind this long-term stroke risk is mostly unknown. Some researchers have proposed that <a href="https://doi.org/10.1212/WNL.0b013e3182267bfa">direct infection of the arteries</a> may be the cause. However, some features of VZV infections suggest that this is not the full picture. A common theme of VZV infections is <a href="https://doi.org/10.1038/nrdp.2015.16">chronic inflammation</a> that spreads beyond the original infection site, which can persist for weeks to months after the virus is no longer detectable and presumably dormant again.</p>
<p>I am a <a href="https://scholar.google.com/citations?user=rH1ZZcwAAAAJ&hl=en">neurovirologist</a>, and <a href="https://www.nvndlab.org">my lab</a> studies how VZV contributes to neurological disorders such as stroke and dementia. In our <a href="https://doi.org/10.1093/infdis/jiac405">recently published research</a>, we found that VZV reactivation triggers the formation of cellular sacs, or exosomes, carrying proteins that contribute to blood clotting and inflammation. An increase in these proteins may lead to an increased risk in stroke.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="TEM image of varicella zoster virus" src="https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=458&fit=crop&dpr=1 600w, https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=458&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=458&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=575&fit=crop&dpr=1 754w, https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=575&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/501604/original/file-20221216-16-rtahtv.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=575&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The varicella zoster virus remains dormant in the nervous system after initial infection.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/varicella-zoster-virus-particle-colored-royalty-free-illustration/91560193">Science Photo Library - Heather Davies/Brand X Pictures via Getty Images</a></span>
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</figure>
<h2>Exosomes carry blood clotting proteins</h2>
<p><a href="https://doi.org/10.1126/science.aau6977">Exosomes</a> are small vesicles, or fluid-filled sacs, made inside cells throughout the body. They’re like duffle bags that carry cargo, such as proteins and nucleic acids, from the cell to distant tissues. Although critical for essential biological functions like communication between cells, exosomes can also play a key role in disease progression and are drug targets for many diseases.</p>
<p>We wanted to see whether shingles patients develop exosomes that carry proteins involved in blood clotting, increasing their risk of stroke. So <a href="https://doi.org/10.1093/infdis/jiac405">we isolated exosomes</a> from the blood of 13 patients at time of shingles rash and compared them to exosomes isolated from healthy donors. </p>
<p>When we analyzed the contents of these exosomes, we found that shingles patients had nine times higher levels of clotting proteins than healthy patients. Moreover, we found the exosomes of shingles patients still had elevated levels of these proteins three months after their initial rash.</p>
<p>To functionally confirm that the contents of these exosomes can induce clotting, we exposed platelets – cell fragments involved in blood clotting – of healthy people to exosomes from either shingles patients or healthy people. We found that exposing platelets to shingles exosomes triggered them to clump together and form aggregates with other types of blood cells, as they would in forming a blood clot.</p>
<p>These findings suggest that exosomes may be a potential mechanism for how the varicella zoster virus increases stroke risk for shingles patients.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Electron micrograph of exosomes on a surface" src="https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=414&fit=crop&dpr=1 600w, https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=414&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=414&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=520&fit=crop&dpr=1 754w, https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=520&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/501609/original/file-20221216-22-5dgp0l.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=520&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Exosomes (marked by the white arrow) can carry a variety of molecules out of a cell.</span>
<span class="attribution"><a class="source" href="https://flic.kr/p/JVTKPN">IBM Research/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<h2>Considering stroke with shingles</h2>
<p>A Food and Drug Administration-approved vaccine to prevent shingles, <a href="https://www.fda.gov/vaccines-blood-biologics/vaccines/shingrix">Shingrix</a>, is available for adults age 50 and older and immunocompromised adults age 18 and older. However, those at highest risk of stroke are under the age of 40 and are ineligible for Shingrix. A large group of these individuals were <a href="https://www.cdc.gov/shingles/hcp/clinical-overview.html">likely not vaccinated</a> for chickenpox as children, as the chickenpox vaccine was only approved in the U.S. in 1995 and uptake by adults was quite low at the time. While vaccination with the chickenpox vaccine <a href="https://doi.org/10.1542/peds.2018-2917">significantly reduces the risk of shingles</a>, it is still possible for a latent infection to reactivate and cause the disease.</p>
<p>While our study provides evidence for a potential way that shingles can cause an increased risk of stroke during and soon after infection, further research on how long this risk persists is needed. We are conducting follow-up studies to evaluate how long patients may have an increased tendency to form blood clots after their shingles infection has resolved. These longitudinal studies will also examine whether exosomes can be used as a biomarker to monitor stroke risk after shingles.</p>
<p>Meanwhile, we hope that our findings may provide a potential target for treatment development, and encourage people to get vaccinated for shingles.</p><img src="https://counter.theconversation.com/content/194627/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Andrew Bubak does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>People with an active case of shingles have up to an 80% higher risk of stroke than those without. The increased risk is highest for patients under 40.Andrew Bubak, Assistant Research Professor of Neurology, University of Colorado Anschutz Medical CampusLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1925972022-10-30T12:21:24Z2022-10-30T12:21:24ZHow COVID-19 damages lungs: The virus attacks mitochondria, continuing an ancient battle that began in the primordial soup<figure><img src="https://images.theconversation.com/files/492284/original/file-20221028-37683-z5drng.jpeg?ixlib=rb-1.1.0&rect=18%2C9%2C2011%2C1578&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Red mitochondria in airway cells become coated with green SARS-COV-2 proteins after viral infection: Researchers discovered that the virus that causes COVID-19 damages lungs by attacking mitochondria.</span> <span class="attribution"><span class="source">(Stephen Archer)</span>, <span class="license">Author provided</span></span></figcaption></figure><iframe style="width: 100%; height: 100px; border: none; position: relative; z-index: 1;" allowtransparency="" allow="clipboard-read; clipboard-write" src="https://narrations.ad-auris.com/widget/the-conversation-canada/how-covid-19-damages-lungs--the-virus-attacks-mitochondria--continuing-an-ancient-battle-that-began-in-the-primordial-soup" width="100%" height="400"></iframe>
<p>Viruses and bacteria have a very long history. Because viruses can’t reproduce without a host, they’ve been attacking bacteria for millions of years. Some of those <a href="https://doi.org/10.1016/0022-5193(67)90079-3">bacteria eventually became mitochondria</a>, synergistically adapting to life within eukaryotic cells (cells that have a nucleus containing chromosomes). </p>
<p>Ultimately, mitochondria became the powerhouses within all human cells. </p>
<p>Fast-forward to the rise of novel coronaviruses like SARS-CoV-2, and the <a href="https://coronavirus.jhu.edu/map.html">global spread of COVID-19</a>. <a href="http://doi.org/10.1056/NEJMoa2002032">Approximately five per cent of people infected with SARS-CoV-2 suffer respiratory failure (low blood oxygen)</a> requiring hospitalization. <a href="https://resources-covid19canada.hub.arcgis.com">In Canada about 1.1 per cent of infected patients (almost 46,000 people) have died</a>. </p>
<p>This is the story of how a team, assembled during the pandemic, recognized the mechanism by which these viruses were causing lung injury and lowering oxygen levels in patients: It is a throwback to the primitive war between viruses and bacteria — more specifically, between this novel virus and the evolutionary offspring of bacteria, our mitochondria.</p>
<p>SARS-CoV-2 is the third novel coronavirus to cause human outbreaks in the 21st century, following <a href="https://www.who.int/health-topics/severe-acute-respiratory-syndrome#tab=tab_1">SARS-CoV in 2003</a> and <a href="https://www.who.int/health-topics/middle-east-respiratory-syndrome-coronavirus-mers#tab=tab_1">MERS-CoV in 2012</a>. We need to better understand how coronaviruses cause lung injury to prepare for the next pandemic.</p>
<h2>How COVID-19 affects lungs</h2>
<p>People with severe COVID-19 pneumonia often arrive at the hospital with unusually low oxygen levels. They have two unusual features distinct from patients with other types of pneumonia:</p>
<ul>
<li>First, they suffer widespread injury to their lower airway (the alveoli, which is where oxygen is taken up). </li>
<li>Second, they shunt blood to unventilated areas of the lung, which is called ventilation-perfusion mismatch. This means blood is going to parts of the lung where it won’t get sufficiently oxygenated.</li>
</ul>
<p>Together, these abnormalities lower blood oxygen. However, the cause of these abnormalities was unknown. In 2020, our team of 20 researchers at three Canadian universities set about to unravel this mystery. <a href="https://doi.org/10.1161/circulationaha.120.047915">We proposed that SARS-CoV-2 worsened COVID-19 pneumonia by targeting mitochondria in airway epithelial cells (the cells that line the airways) and pulmonary artery smooth muscle cells</a>. </p>
<p>We already knew that mitochondria are not just the powerhouse of the cell, but also its main consumers and <a href="https://doi.org/10.1056/nejmra050002">sensors of oxygen</a>. Mitochondria control the process of programmed cell death (called apoptosis), and they regulate the distribution of blood flow in the lung by a mechanism called hypoxic pulmonary vasoconstriction. </p>
<p>This mechanism has an important function. It directs blood away from areas of pneumonia to better ventilated lobes of the lung, which optimizes oxygen-uptake. By damaging the mitochondria in the smooth muscle cells of the pulmonary artery, the virus allows blood flow to continue into areas of pneumonia, which also lowers oxygen levels. </p>
<p>It appeared plausible that SARS-CoV-2 was damaging mitochondria. The results of this damage — an increase in apoptosis in airway epithelial cells, and loss of hypoxic pulmonary vasoconstriction — were making lung injury and hypoxemia (low blood oxygen) worse. </p>
<p>Our discovery, <a href="https://doi.org/10.1016/j.redox.2022.102508">published in <em>Redox Biology</em></a>, explains how SARS-CoV-2, the coronavirus that causes COVID-19 pneumonia, reduces blood oxygen levels. </p>
<p>We show that SARS-CoV-2 kills airway epithelial cells by damaging their mitochondria. This results in fluid accumulation in the lower airways, interfering with oxygen uptake. We also show that SARS-CoV-2 damages mitochondria in the pulmonary artery smooth muscle cells, which inhibits hypoxic pulmonary vasoconstriction and lowers oxygen levels. </p>
<h2>Attacking mitochondria</h2>
<p>Coronaviruses damage mitochondria in two ways: by regulating mitochondria-related gene expression, and by direct protein-protein interactions. When SARS-CoV-2 infects a cell, it hijacks the host’s protein synthesis machinery to make new virus copies. However, these <a href="http://doi.org/10.1038/s41586-020-2286-9">viral proteins also target host proteins, causing them to malfunction</a>. We soon learned that many of the host cellular proteins targeted by SARS-CoV-2 were in the mitochondria. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Cartoon with three panels: a coronavirus shooting arrows at mitochondria and spitting them in two; lungs and contrasting healthy and damaged lung cells; an oxygen meter with the needle in the red zone; and a human silhouette showing airways" src="https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=384&fit=crop&dpr=1 600w, https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=384&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=384&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=483&fit=crop&dpr=1 754w, https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=483&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/490891/original/file-20221020-25-rozyzy.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=483&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">How SARS-CoV-2 targets mitochondria to kill lung cells and prevent oxygen sensing.</span>
<span class="attribution"><span class="source">(drawn by Brooke Ring)</span>, <span class="license">Author provided</span></span>
</figcaption>
</figure>
<p>Viral proteins fragment the mitochondria, depriving cells of energy and interfering with their oxygen-sensing capability. The viral attack on mitochondria starts within hours of infection, turning on genes that break the mitochondria into pieces (called mitochondrial fission) and make their membranes leaky (an early step in apoptosis called mitochondrial depolarization). </p>
<p>In our experiments, we didn’t need to use a replicating virus to damage the mitochondria — simply introducing single SARS-CoV-2 proteins was enough to cause these adverse effects. This mitochondrial damage also occurred with other coronaviruses that we studied. </p>
<p>We are now developing drugs that may one day counteract COVID-19 by blocking mitochondrial fission and apoptosis, or by preserving hypoxic pulmonary vasoconstriction. Our drug discovery efforts have already enabled us to identify <a href="https://doi.org/10.1096/fj.201901467r">a promising mitochondrial fission inhibitor, called Drpitor1a</a>. </p>
<p>Our team’s infectious diseases expert, Gerald Evans, notes that this discovery also has the potential to help us understand Long COVID. “The predominant features of that condition — fatigue and neurologic dysfunction — could be due to the lingering effects of mitochondrial damage caused by SARS-CoV-2 infection,” he explains.</p>
<h2>The ongoing evolutionary battle</h2>
<p>This research also has an interesting evolutionary angle. Considering that <a href="https://doi.org/10.1016/0022-5193(67)90079-3">mitochondria were once bacteria, before being adopted by cells back in the primordial soup</a>, our findings reveal an Alien versus Predator scenario in which viruses are attacking “bacteria.”</p>
<p>Bacteria are regularly attacked by viruses, called bacteriophages, that need a host to replicate in. The bacteria in turn fight back, using an ancient form of immune system called the CRISPR-cas system, that chops up the viruses’ genetic material. Humans have recently exploited this CRISPR-cas system for <a href="https://www.synthego.com/blog/gene-editing-nobel-prize">a Nobel Prize-winning gene editing discovery</a>. </p>
<p>The ongoing competition between bacteria and viruses is a very old one; and recall that our mitochondria were once bacteria. So perhaps it’s not surprising at all that SARS-CoV-2 attacks our mitochondria as part of the COVID-19 syndrome.</p>
<h2>Pandemic pivot</h2>
<p>The original team members on this project are heart and lung researchers with expertise in mitochondrial biology. In early 2020 we pivoted to apply that in another field — virology — in an effort to make a small contribution to the COVID-19 puzzle. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A grid of photographs of 25 scientists, and the three collaborating institutions (Queen's University, the Vaccine and Infectious Disease Organization (VIDO) and University of Toronto)" src="https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=342&fit=crop&dpr=1 600w, https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=342&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=342&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=429&fit=crop&dpr=1 754w, https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=429&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/492257/original/file-20221028-27-7vme8l.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=429&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The COVID team: The face of research. The diverse team includes members who came to Canada from India, Iran, England, Brazil, Iraq, China and Taiwan to pursue research here.</span>
<span class="attribution"><span class="source">(Stephen Archer)</span>, <span class="license">Author provided</span></span>
</figcaption>
</figure>
<p><a href="https://youtu.be/cJlAsFoTWLg">The diverse team we put together also brought expertise</a> in mitochondrial biology, cardiopulmonary physiology, SARS-CoV-2, <a href="https://www.phgfoundation.org/blog/what-is-transcriptomics">transcriptomics</a>, synthetic chemistry, molecular imaging and infectious diseases. </p>
<p>Our discovery owes a lot to our virology collaborators. Early in the pandemic, University of Toronto virologist Gary Levy offered us a mouse coronavirus (MHV-1) to work with, which we used to make a model of COVID-19 pneumonia. Che Colpitts, a virologist at Queen’s University, helped us study the mitochondrial injury caused by another human beta coronavirus, HCoV-OC43. </p>
<p>Finally, Arinjay Banerjee and his expert SARS-CoV-2 virology team at <a href="https://www.vido.org">Vaccine and Infectious Disease Organization (VIDO)</a> in Saskatoon performed key studies of human SARS-CoV-2 in airway epithelial cells. VIDO is one of the few Canadian centres equipped to handle the highly infectious SARS-CoV-2 virus. </p>
<p>Our team’s super-resolution microscopy expert, Jeff Mewburn, notes the specific challenges the team had to contend with.</p>
<p>“Having to follow numerous and extensive COVID-19 protocols, they were still able to exhibit incredible flexibility to retool and refocus our laboratory specifically on the study of coronavirus infection and its effects on cellular/mitochondrial functions, so very relevant to our global situation,” he said.</p>
<p>Our discovery will hopefully be translated into new medicines to counter future pandemics.</p><img src="https://counter.theconversation.com/content/192597/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Stephen L Archer receives funding from the Canadian Institutes of Health Research for research on COVID-19. Dr Archer is convector on a patent for small molecule inhibitors of mitochondrial fission.</span></em></p>COVID-19 causes lung injury and lowers oxygen levels in patients because the SARS-CoV-2 virus attacks cells’ mitochondria. This attack is a throwback to a primitive war between viruses and bacteria.Stephen L Archer, Professor, Head of Department of Medicine, Queen's University, OntarioLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1920282022-10-09T07:39:22Z2022-10-09T07:39:22ZNigeria’s missing virus hunters: university decline robs country of virologists<figure><img src="https://images.theconversation.com/files/488727/original/file-20221007-26-y700xw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">shutterstock</span></span></figcaption></figure><p><em>Nigeria’s university system witnessed its <a href="https://www.jstor.org/stable/1166618#metadata_info_tab_contents">golden era</a> between the 1950s and 1980s. It produced globally <a href="https://theconversation.com/akin-mabogunje-nigerian-urban-geographer-who-mapped-the-origin-and-trends-of-african-cities-190378">celebrated academics </a> and <a href="https://theconversation.com/david-olufemi-olaleye-erudite-virologist-excellent-mentor-and-academic-giant-166199">virologists</a>. But the story has changed. Under funding of the university system, inadequate support for research and lack of commitment to the development of science and technology by the government are robbing the nation of quality academics. Virologists are among them. Renowned virologist, Oyewale Tomori, who graduated in the 1970s, sets out how it was then, why the country is where it is now and what it can do to restore its lost glory in science and technology education.</em></p>
<hr>
<h2>What’s the history of training virologists in Nigeria?</h2>
<p>Although modern virology began with the discovery between 1915 and 1917 of bacteriophages (that is, <a href="https://scholar.google.com/scholar?q=DOI:https://doi.org/10.1016/j.cmi.2018.12.003&hl=en&as_sdt=0&as_vis=1&oi=scholart">viruses that infect bacteria </a>, virology only became a discipline on its own in the last 50 years. </p>
<p>The discipline can be divided into the biology of viruses (molecular biology and biochemistry) and viral diseases (physiology, epidemiology, and clinical aspects of virus diseases). One branch deals with the study of the nature and properties of the virus, while the second is focused on the diseases caused by viruses and the interplay of the factors (human, animal, virus and the environment) that result in the emergence and reemergence of viral diseases. </p>
<p>Today, a thorough study of virology encompasses the <a href="https://www.cdc.gov/onehealth/index.html#:%7E:text=One%20Health%20is%20a%20collaborative,plants%2C%20and%20their%20shared%20environment">One Health concept</a>. This takes into account the interactions between humans and animals and the environment.</p>
<p>The first set of Nigerian virologists was trained outside the country. Local training of virologists started in the early 1970s, at the University of Ibadan. It was the sole training centre for virologists until the late 1990s. </p>
<p>Today, <a href="https://punchng.com/nigeria-has-only-200-virologists-expert-laments/">there are about 200 virologists in Nigeria</a>. Is this number enough?</p>
<p>Answering the question isn’t the same as measuring, for example, the ideal “doctor to patient” ratio. This is because virologists are researchers, so the headline number isn’t the main issue. Rather it’s whether those trained as virologists are functioning effectively and maximally. </p>
<p>Suffice to say that Nigeria needs more virologists given the size of the country, and the number of endemic viral infections prevalent in it. Annually, the country reports severe outbreaks of virus diseases, such as Lassa Fever, yellow fever and measles.</p>
<p>You need virolgists to be ahead of the emergence of viral disease outbreaks. </p>
<p>But the high cost of equipment and reagents, as well as other facilities for conducting virus studies have limited the output of trained virologists by the Nigerian university system. </p>
<p>Currently, the country has more virologists specialising as molecular virologists, rather than experts on the epidemiology and clinical aspects of viral diseases. And poor collaboration between laboratory scientists, epidemiologists and clinicians has robbed Nigeria of getting the needed balance between molecular virologists and those studying viral diseases. There is a disconnect between the study of viruses and the diseases they cause. We have expert virologists with little knowledge of how to control the diseases caused by viruses. </p>
<p>Virologists who will be relevant and contribute to improving the health of the society, must use their knowledge and expertise to prevent and control viral disease, otherwise they become a precious ornament of little use to someone dying of a viral disease. </p>
<p>Nigeria, a disease ridden society, has no place for virologists who discover a virus but can’t decipher what it does. Or are unable to use their knowledge to mitigate the devastation of a viral disease outbreak. </p>
<h2>What’s different now in the training of virologists?</h2>
<p>When I trained as a virologist at the University of Ibadan in South West Nigeria, the training was comprehensive. It involved both broad-based field work as well as laboratory investigation. </p>
<p>In the past, in addition to employing available techniques (antigen-antibody studies and animal experimentation) to identify and classify viruses, a detailed epidemiological study of the diseases caused by the virus was also carried out. </p>
<p>This was a One Health concept that considered the pathogen, the person, the animal, and the environment in the study of viruses and the diseases they cause. This provided information needed for the control and prevention of the disease. </p>
<p>Today, the focus is principally on studying and dissecting the virus, using more modern and highly sophisticated techniques, like <a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/genome-sequencing">genomic sequencing</a>. </p>
<p>A host of hurdles stand in the way of building a bigger cohort of virologists in Nigeria.</p>
<p>Firstly, the lack of modern facilities in laboratories and the poor state of basic infrastructure and other resources (such as electricity and reagents) are working against research development. You cannot run genetic sequencing or even sterilise your equipment using a candle as your source of power.</p>
<p>Secondly, budgetary allocation to education is generally poor – at all levels, including the secondary school system. </p>
<p>Thirdly, and unfortunately, the <a href="https://guardian.ng/features/despite-tetfund-intervention-research-in-tertiary-institutions-still-poor-experts-say/">Nigerian government is not committed to funding research</a>. Financial support for science and research remains pathetic. This has led to the deterioration in the quantity and quality of trained virologists at Nigeria’s universities. The oases of excellence in the Nigerian desert of research landscape are largely funded by grants from external bodies and agencies. </p>
<p>But for how long are you going to depend on external grants to fund your research and development? It is like Africa whining and crying for equity when, for example, COVID-19 vaccines were not available for our populations. You do not beg for equity, you fight for it. You use your resources responsibly to contribute to equity, and not just be a consumer of the crumbs of equity.</p>
<p>On top of this, we have corruption and examination malpractices undermining the very foundation of integrity and probity, the pillars on which science and research stand. Consequently, our university system is neither able to retain responsible academics, nor attract the right kind of prospective students imbued with responsibility. </p>
<p>Add to these hurdles the lack of interest of many students in science and technological education. </p>
<h2>What’s missing?</h2>
<p>Sustained funding, infrastructure, facilities (regular power supply), and national government support for and sustained commitment to research. </p>
<p>There is a general national disdain for science and technology. There is also a national failure to fully recognise that science and technology are needed for the socio-economic transformation of Nigeria.</p>
<p>The government should invest in science, technology, research and development. </p>
<h2>How has this affected Nigeria’s ability to produce cutting-edge research?</h2>
<p>Adversely. </p>
<p>We are a nation consuming other countries’ returns on investment in science, research and technology. Rather than investing in research and contributing to global development through science and research, we have resorted to begging for the crumbs of equity. </p>
<p>We are only ready to consume other people’s returns on investments on science and research. </p>
<h2>What needs to be done?</h2>
<p>Go back to basics. Invest in research, science and technology. </p>
<p>Nigeria should create an enabling environment for scientists to function effectively and maximally. The nation should commit to using research outcomes in science and technology as the medium for transforming our society to a developed nation. If Nigeria refuses to fund research especially in science and technology, we will remain at the blunt-edge, rather than the cutting-edge of research, science and technology. We will not have the body of knowledge that can help us to address the nation’s health and other challenges.</p><img src="https://counter.theconversation.com/content/192028/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Oyewale Tomori does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Financial support for science and research in Nigeria remains pathetic. This has led to the deterioration in the quantity and quality of trained virologists at universities.Oyewale Tomori, Fellow, Nigerian Academy of ScienceLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1899492022-09-15T12:25:40Z2022-09-15T12:25:40ZViruses may be ‘watching’ you – some microbes lie in wait until their hosts unknowingly give them the signal to start multiplying and kill them<figure><img src="https://images.theconversation.com/files/484664/original/file-20220914-25-l0cplf.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2309%2C1299&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Phages can sense bacterial DNA damage, which triggers them to replicate and jump ship.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/bacteriophage-infecting-bacterium-royalty-free-image/992263464">Design Cells/iStock via Getty Images Plus</a></span></figcaption></figure><p>After more than two years of the COVID-19 pandemic, you might picture a virus as a nasty spiked ball – a mindless killer that gets into a cell and hijacks its machinery to create a gazillion copies of itself before bursting out. For many viruses, including the <a href="https://doi.org/10.1038/s41579-020-00468-6">coronavirus that causes COVID-19</a>, the “mindless killer” epithet is essentially true.</p>
<p>But there’s more to virus biology than meets the eye.</p>
<p>Take HIV, the virus that causes <a href="https://doi.org/10.1002/eji.200737441">AIDS</a>. HIV is a <a href="https://doi.org/10.1101%2Fcshperspect.a006882">retrovirus</a> that does not go directly on a killing spree when it enters a cell. Instead, it integrates itself into your chromosomes and chills, waiting for the right moment to command the cell to make copies of it and burst out to infect other immune cells and eventually cause AIDS.</p>
<p>Exactly what moment HIV is waiting for is still an <a href="https://doi.org/10.1016/j.cell.2018.04.005">area of active study</a>. But research on other viruses has long hinted that these pathogens can be quite “thoughtful” about killing. Of course, viruses cannot think the way you and I do. But, as it turns out, evolution has endowed them with some pretty elaborate decision-making mechanisms. Some viruses, for instance, will choose to leave the cell they have been residing in if they detect DNA damage. Not even viruses, it appears, like to stay in a sinking ship.</p>
<p><a href="https://scholar.google.com/citations?user=T1I1sNAAAAAJ&hl=en">My</a> <a href="https://erilllab.umbc.edu/">laboratory</a> has been studying the molecular biology of <a href="https://doi.org/10.4161%2Fbact.1.1.14942">bacteriophages</a>, or phages for short, the viruses that infect bacteria, for over two decades. Recently, my colleagues and I <a href="https://doi.org/10.3389/fmicb.2022.918015">have shown</a> that phages can listen for key cellular signals to help them in their decision-making. Even worse, they can use the cell’s own “ears” to do the listening for them.</p>
<h2>Escaping DNA damage</h2>
<p>If the enemy of your enemy is your friend, phages are certainly your friends. Phages <a href="https://doi.org/10.4161%2Fbact.1.1.14942">control bacterial populations</a> in nature, and clinicians are increasingly using them to <a href="https://doi.org/10.1038/s41591-019-0437-z">treat bacterial infections</a> that do not respond to antibiotics.</p>
<p>The best studied phage, <a href="https://doi.org/10.1016/j.virol.2015.02.010">lambda</a>, works a bit like HIV. Upon entering the bacterial cell, lambda decides whether to replicate and kill the cell outright, like most viruses do, or to integrate itself into the cell’s chromosome, as HIV does. If the latter, lambda harmlessly replicates with its host each time the bacteria divides. </p>
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<figcaption><span class="caption">This video shows a lambda phage infecting <em>E. coli</em>.</span></figcaption>
</figure>
<p>But, like HIV, lambda is not just sitting idle. It uses a special protein called CI like a stethoscope to listen for signs of DNA damage within the bacterial cell. If the bacterium’s DNA gets compromised, that’s bad news for the lambda phage nested within it. Damaged DNA leads straight to evolution’s landfill because it’s useless for the phage that needs it to reproduce. So lambda turns on its replication genes, makes copies of itself and bursts out of the cell to look for more undamaged cells to infect.</p>
<h2>Tapping the cell’s communication system</h2>
<p>Some phages, instead of gathering intel with their own proteins, tap the infected cell’s very own DNA damage sensor: LexA.</p>
<p>Proteins like CI and LexA are <a href="https://doi.org/10.1016/j.jmb.2019.04.011">transcription factors</a> that turn genes on and off by binding to specific genetic patterns within the DNA instruction book that is the chromosome. Some phages like Coliphage 186 have figured out that they don’t need their own viral CI protein if they have a short DNA sequence in their chromosomes that bacterial LexA can bind to. Upon detecting DNA damage, LexA will activate the phage’s replicate-and-kill genes, essentially double-crossing the cell into committing suicide while allowing the phage to escape.</p>
<p>Scientists first reported CI’s role in phage decision-making <a href="https://doi.org/10.1038/294217a0">in the 1980s</a> and Coliphage 186’s counterintelligence trick <a href="https://doi.org/10.1074/jbc.273.10.5708">in the late 1990s</a>. Since then, there have been a few other reports of phages tapping bacterial communication systems. One example is <a href="https://doi.org/10.1038/sj.emboj.7600826">phage phi29</a>, which exploits its host’s transcription factor to detect when the bacterium is getting ready to generate a spore, or a kind of bacterial egg <a href="https://doi.org/10.1023/A:1020561122764">capable of surviving extreme environments</a>. Phi29 instructs the cell to package its DNA into the spore, killing the budding bacteria once the spore germinates.</p>
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<figcaption><span class="caption">Transcription factors turn genes on and off.</span></figcaption>
</figure>
<p>In our <a href="https://doi.org/10.3389/fmicb.2022.918015">recently published research</a>, my colleagues and I show that several groups of phages have independently evolved the ability to tap into yet another bacterial communication system: the CtrA protein. CtrA integrates multiple internal and external signals to set in motion different developmental processes in bacteria. Key among these is the production of bacterial appendages called <a href="https://doi.org/10.1007/s12275-017-7369-4">flagella and pili</a>. Turns out, these phages attach themselves to the pili and flagella of bacteria in order to infect them.</p>
<p>Our leading hypothesis is that phages use CtrA to guesstimate when there will be enough bacteria nearby sporting pili and flagella that they can readily infect. A pretty smart trick for a “mindless killer.”</p>
<p>These are not the only phages that make elaborate decisions – all without the benefit of even having a brain. Some phages that infect <em>Bacillus</em> bacteria produce a small molecule each time they infect a cell. The phages can sense this molecule and use it to <a href="https://doi.org/10.1016/j.cub.2021.08.072">count the number of phage infections</a> taking place around them. Like alien invaders, this count helps decide when they should switch on their replicate-and-kill genes, killing only when hosts are relatively abundant. This way, the phages make sure that they never run out of hosts to infect and guarantee their own long-term survival.</p>
<h2>Countering viral counterintelligence</h2>
<p>You may be wondering why you should care about the counterintelligence ops run by bacterial viruses. While bacteria are very different from people, the viruses that infect them are <a href="https://doi.org/10.1128/MMBR.00193-20">not that different</a> from the viruses that infect humans. Pretty much <a href="https://doi.org/10.1016/j.virol.2012.09.017">every single trick</a> played by phages has later been shown to be used by human viruses. If a phage can tap bacterial communication lines, why wouldn’t a human virus tap yours?</p>
<p>So far, researchers don’t know what human viruses could be listening for if they hijack these lines, but plenty of options come to mind. I believe that, like phages, human viruses could potentially be able to count their numbers to strategize, detect cell growth and tissue formation and even monitor immune responses. For now, these possibilities are only speculation, but scientific investigation is underway.</p>
<p>Having viruses listening to your cells’ private conversations is not the rosiest of pictures, but it’s not without a silver lining. As intelligence agencies all around the world know well, counterintelligence works only when it’s covert. Once detected, the system can very easily be exploited to feed misinformation to your enemy. Similarly, I believe that future antiviral therapies may be able to combine conventional artillery, like antivirals that prevent viral replication, with information warfare trickery, such as making the virus believe the cell it is in belongs to a different tissue. </p>
<p>But, hush, don’t tell anybody. Viruses could be listening!</p><img src="https://counter.theconversation.com/content/189949/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ivan Erill receives funding from the US National Science Foundation</span></em></p>Phages, or viruses that infect bacteria, can lie dormant within chromosomes until they’re triggered to replicate and burst out of their hosts.Ivan Erill, Associate Professor of Biological Sciences, University of Maryland, Baltimore CountyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1887642022-09-05T18:36:09Z2022-09-05T18:36:09ZHIV patients in Botswana get adequate treatment but not all of them – one group is slipping through the cracks<figure><img src="https://images.theconversation.com/files/481068/original/file-20220825-14-j8bh53.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Franco Volpato/Shutterstock</span></span></figcaption></figure><p>HIV remains a major public health challenge globally. Around <a href="https://www.unaids.org/en/resources/fact-sheet">38 million</a> people are estimated to be living with the infection. Sub-Saharan Africa bears the brunt of the HIV epidemic. Close to two thirds of the HIV cases are in the region. </p>
<p>But huge strides have been made in curbing the epidemic. One of the keys to this has been the introduction of antiretroviral therapy (ART). It’s resulted in people with HIV living long, productive lives and reducing the risks of HIV transmission. </p>
<p>HIV has a high mutation rate, however. As a result, there is evidence of HIV variants with resistance to almost all available antiretroviral drugs. The development of variants with drug resistant mutations is a major challenge to the success of ART – and therefore to efforts to achieve the UN goal of <a href="https://www.unaids.org/en/resources/campaigns/World-AIDS-Day-Report-2014">ending AIDS by 2030</a>.</p>
<p>In developing countries, screening for HIV drug resistant variants is done only when patients who are on treatment have high viral loads – over 1,000 copies/ml, as per the World Health Organization <a href="https://www.who.int/publications/i/item/9789241507196">guidelines</a>. This means drug resistant HIV variants in patients with low viral loads aren’t detected. This is the case in many countries in sub-Saharan Africa – including Botswana.</p>
<p>We <a href="https://www.researchgate.net/publication/358958674_HIV-1_drug_resistance_mutations_among_individuals_with_low-level_viraemia_while_taking_combination_ART_in_Botswana">set out to establish</a> three things.</p>
<p>Firstly, what percentage of patients on ART had low HIV viral loads. This is data that’s never been collected before. Secondly, we wanted to determine HIV drug resistant mutations in this cohort of patients. The third thing we set to establish is whether there’s a connection between patients with low viral loads and treatment failure. This is known as virologic failure.</p>
<p>Answering these three questions has given us a much deeper understanding of where a country like Botswana stands in its efforts to eliminate HIV. As a result of our research we have a better understanding of how many people with HIV have low viral loads, how serious a threat we face from drug resistant HIV variants and finally how many people with low viral levels are at risk of treatment failure. </p>
<p>We found that people with low viral loads were just as likely to harbour drug resistant HIV variants as people with high viral loads. This matters because it points to the need to change how people with HIV who are on ART are managed in developing countries. </p>
<p>We recommend that patients on ART with detectable viral loads above 50 copies/ml be further investigated to ensure that they don’t harbour drug resistant HIV variants. </p>
<h2>What we found</h2>
<p><strong>Number of HIV patients on ART with low viral load:</strong> Our study looked at a cohort of 6,078 people with HIV from across Botswana who were receiving combination antiretroviral therapy. We narrowed this down to 4,443 people who had been on ART treatment for at least six months. </p>
<p>Only 8% had viral loads of more than 50 copies/ml. Testing for mutations only happens on patients with viral loads of over 1,000 copies/ml, which means that this group isn’t being screened.</p>
<p>The figure of 8% may seem low. But it means that this cohort either has a resistant variant, or their treatment isn’t working.</p>
<p><strong>Prevalence of drug resistant mutations:</strong> We sequenced the HIV in the patients with low viral loads as well as those with viral loads above 1,000 copies/ml. We found no difference in the prevalence of HIV drug resistant mutations between the two patient groups. This indicates that patients with low HIV viral loads are just as likely to harbour HIV variants with drug resistance mutations as those with high viral loads.</p>
<p><strong>Treatment failure:</strong> A select group of the patients with low HIV viral loads were followed up for at least a year. We found that there was a statistically significant association of low level HIV viral load with subsequent virological (or treatment) failure. Our results show that patients with a low HIV viral load are more likely to experience virological failure.</p>
<p>Current treatment guidelines describe virologic failure as viral loads above 1,000 copies/ml. Our results challenge this. </p>
<h2>Going forward</h2>
<p>Our results echo the views expressed by others who have <a href="https://www.frontiersin.org/articles/10.3389/fmed.2022.939261/full">looked at this issue</a>. Like them, we recommend that the HIV treatment guidelines in developing countries be improved to ensure that patients with low HIV viral load while on ART get the necessary attention. </p>
<p>In developed countries, screening for drug resistant HIV variants is done when people start ART. Drug resistance screening is also done whenever a patient on treatment has a detectable viral load. </p>
<p>The same approach should be applied in developing countries. </p>
<p>Patients should also have a follow-up viral load test which – if the virus is still detectable – should lead to sequencing of the HIV variants they harbour. If found to have a drug resistant variant, the patient should be switched to an appropriate ART regimen. </p>
<p>If they are found not to harbour HIV drug resistant variants, the patient should undergo intensive adherence counselling because this could point to treatment failure. </p>
<p>Scientists and funders must invest time and resources to develop more sensitive HIV drug resistant assays that can sequence HIV in samples with low viral loads. This is currently a limiting factor as most of the available assays don’t work well with samples with low viral loads.</p><img src="https://counter.theconversation.com/content/188764/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Simani Gaseitsiwe receives funding from : Wellcome Trust, NIH, EDCTP, Bill and Melinda Gates Foundation.
</span></em></p>Patients with low HIV viral loads are just as likely to harbour HIV variants with drug resistance mutations as those with high viral loads.Simani Gaseitsiwe, Principal Investigator and Research Associate at Botswana Harvard AIDS Institute Partnership, Sub-Saharan African Network for TB/HIV Research Excellence (SANTHE)Licensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1871152022-08-08T15:47:02Z2022-08-08T15:47:02ZNew COVID variants could emerge from animals or from people with chronic infections – but it’s not cause for panic<figure><img src="https://images.theconversation.com/files/476948/original/file-20220801-38718-poy2ea.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C5991%2C3287&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/corona-virus-mutation-medical-3d-illustration-1892875636">peterschreiber.media/Shutterstock</a></span></figcaption></figure><p>As the COVID pandemic rolls on, we’re becoming all too familiar with the continued emergence of new variants. Some can <a href="https://pubmed.ncbi.nlm.nih.gov/34989238/">thwart immunity</a> from vaccines and prior infections, increasing their capacity to disrupt our everyday lives. But where do new variants actually come from?</p>
<p>Variants develop through changes in the genetic code of the virus. This happens most commonly through <a href="https://theconversation.com/coronavirus-variants-how-did-they-evolve-and-what-do-they-mean-153405">mutations</a>, essentially copy errors in the virus’ genetic information. Variants of concern are variants that have been identified to have a significant impact on transmissibility, severity of disease or immunity, likely to change the epidemiological situation of the pandemic.</p>
<p>Each time we’re infected with SARS-CoV-2 (the virus that causes COVID), our bodies produce a large number of virus particles with a range of genetic differences to the original infecting virus and to each other. Many of these mutations will have no effect on the virus. </p>
<p>Occasionally, however, mutations will occur that give the virus an advantage. For example, <a href="https://www.nature.com/articles/d41586-021-02275-2">delta</a> was more transmissible than earlier variants because of a mutation in its spike protein (a protein on the surface of SARS-CoV-2) allowing the virus to infect our cells more easily.</p>
<p>Even though we know a lot about how mutation occurs, it’s incredibly difficult to pinpoint where specific variants came from. But recent studies have investigated potential sources of new SARS-CoV-2 variants, including people who experience <a href="https://www.nature.com/articles/s41591-022-01882-4">chronic COVID infections</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/33892621/">animals</a>.</p>
<h2>Chronic infections</h2>
<p>A chronic infection is where a person is actively infected with SARS-CoV-2 for a <a href="https://www.nature.com/articles/s41591-022-01882-4">long period of time</a>. This is different to long COVID, where symptoms persist well after the patient has recovered from the initial infection.</p>
<p>Chronic cases are rare and, to date, all documented cases have been in people with severely suppressed immune systems. These might be people undergoing treatment for cancer or following an organ transplant, for example.</p>
<p>Several <a href="https://www.nature.com/articles/s41586-021-03291-y">studies</a> have shown that the <a href="https://journals.asm.org/doi/10.1128/mSphere.00244-21#:%7E:text=In%20the%20present%20study%2C%20we,being%20accumulated%20after%20164%20days">rate of mutation</a> in these patients is higher than in those who are infected for a shorter time. Immunocompromised patients have a reduced immune response to infection and are often undergoing a range of treatments, both factors which are thought to allow a broader variety of mutations to develop. This is compounded by the longer period of time for which they may be infected.</p>
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Read more:
<a href="https://theconversation.com/coronaviruses-a-brief-history-135506">Coronaviruses – a brief history</a>
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<p>While new COVID variants do appear more likely to form in patients with chronic infections, the good news is they don’t seem to pose a significant threat. </p>
<p>In a <a href="https://www.nature.com/articles/s41591-022-01882-4">recent study</a> that looked at 27 chronically infected patients, there was no clear pattern of mutations. And when comparing mutations identified in the chronic patients with existing <a href="https://www.who.int/activities/tracking-SARS-CoV-2-variants">variants of concern</a>, the chronic infections often lacked key mutations repeatedly identified in the variants of concern.</p>
<p>The researchers suggest the the majority of variants arising from chronically infected patients enhance virus replication, but are not characterised by improved transmission. This means they’re good at replicating in an infected person, but not as good at spreading from person to person. </p>
<p>The study demonstrated that there was no evidence of onward transmission from the patients with chronic infections to other people, which would be essential for a new variant to take hold and become a variant of concern. Although the authors note this may be due to human behaviour, rather than virus evolution, as immunosuppressed patients are likely to be confined to their homes. </p>
<p>That said, most variants of concern <a href="https://pubmed.ncbi.nlm.nih.gov/35150638/">possess mutations</a> that enhance transmission rather than replication, so it seems unlikely that these patients are significant sources of variants of concern.</p>
<h2>Animal reservoirs</h2>
<p>SARS-CoV-2 is likely to have been originally transmitted to humans via <a href="https://www.science.org/doi/10.1126/science.abp8715">an animal market in China</a>, and throughout the pandemic, we’ve learned that the virus can infect <a href="https://pubmed.ncbi.nlm.nih.gov/32269068/">a variety of animals</a>. </p>
<p>So another suggestion is that animals <a href="https://www.pnas.org/doi/10.1073/pnas.2105253118">could be the source</a> of new SARS-CoV-2 variants. The idea is they contract the virus from humans, which then mutates during infection in the animal host, before spreading back to humans.</p>
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<img alt="A mink in the wild." src="https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/476958/original/file-20220801-82620-uyyv4z.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Could animals be a breeding ground for new COVID variants?</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/jung-american-mink-on-green-grass-1792096061">An inspiration/Shutterstock</a></span>
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<p>A species jump (or “zoonosis”) can only occur when <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7114646/">multiple factors</a> align. These include virological factors (for example, mutations that allow infection of human cells) and environmental factors (for example, close contact with infected animals). Zoonosis is not common, but is becoming more regular due to <a href="https://pubmed.ncbi.nlm.nih.gov/35483403/">climate change and deforestation</a>, which put more animals in contact with humans.</p>
<p>One <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8702434/">study</a> analysed the genetic code of omicron and showed high levels of similarity in the spike protein with that of mouse coronaviruses. The authors suggest the omicron variant may have occurred as a result of a human-to-mouse infection, mutation in the infected mouse, followed by transmission back to humans.</p>
<p>But often, when a virus infects a new host, such as a human, it’s unable <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394705/">to be transmitted further</a> to other humans. The virus has to quickly adapt to allow it to thrive in the new host and go on to infect others. Indeed, where <a href="https://www.science.org/doi/10.1126/science.abe5901">animal-to-human transmission</a> of COVID occurred on Dutch mink farms, while we did see <a href="https://www.nature.com/articles/s41467-022-30698-6">the virus mutate</a>, there was no evidence of further transmission from the farm workers into the wider community.</p>
<p>Similarly, we’ve observed many instances of people infected <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6992886/">with bird flu</a> through prolonged close contact with birds. But there have been very few events of further transmission to other humans. </p>
<p>So although new variants may form in animals occasionally, it seems unlikely that they’re being re-transmitted back to humans and spreading.</p>
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<strong>
Read more:
<a href="https://theconversation.com/human-catches-covid-from-a-cat-heres-why-this-new-evidence-is-not-cause-for-panic-186233">Human catches COVID from a cat – here's why this new evidence is not cause for panic</a>
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<p>While we can know geographically where new SARS-CoV-2 variants were first detected, it’s almost certain we’ll never know exactly where they come from. But as virus evolution is based on a combination of chance events such as mutation and human behaviour, it’s most likely that variants of concern are formed in a wide range of infected patients across the world. </p>
<p>With so many people being infected at once, many living in dense cities and travelling across the globe, the chances of viral evolution and onward spread of new mutants are increased. If large numbers of infections continue globally, more variants will continue to arise.</p><img src="https://counter.theconversation.com/content/187115/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Grace C Roberts works at the University of Leeds and receives funding from the MRC. </span></em></p>Animal reservoirs and people who experience chronic COVID infections could potentially see the emergence of new variants. But these variants aren’t necessarily cause for concern.Grace C Roberts, Research Fellow in Virology, University of LeedsLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1821542022-05-16T19:59:38Z2022-05-16T19:59:38ZGot COVID again? Your symptoms may be milder, but this won’t always be the case<figure><img src="https://images.theconversation.com/files/462655/original/file-20220512-26-f64l6d.jpg?ixlib=rb-1.1.0&rect=187%2C104%2C6762%2C4448&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/sad-tired-young-woman-massaging-temples-1927170659">Shutterstock</a></span></figcaption></figure><p>So, you’re starting to feel unwell. Your throat hurts, your head aches, you feel tired and you’ve developed a cough. </p>
<p>You’ve recently had COVID but as we now know, it’s <a href="https://theconversation.com/covid-reinfections-are-they-milder-and-do-they-strengthen-immunity-176592">possible to be reinfected</a>. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1521598006683971586"}"></div></p>
<p>But how sick will you get the second time? </p>
<p>While your symptoms are likely to be less severe, in some cases they can be worse. Here’s what we know so far.</p>
<h2>After COVID, you don’t need to test for 12 weeks</h2>
<p>Current <a href="https://www.qld.gov.au/health/conditions/health-alerts/coronavirus-covid-19/stay-informed/i-have-covid/after-having-covid-19">guidelines</a> define you as a “cleared case” for <a href="https://www.healthdirect.gov.au/covid-19/recovery-and-returning-to-normal-activities#:%7E:text=Recovered%20cases%20don't%20need,be%20tested%20for%20COVID%2D19.">12 weeks after</a> ending COVID isolation. If you develop COVID-like symptoms in that 12 weeks, you don’t need to be tested. </p>
<p>The science behind this 12-week timeframe is evolving. The original idea was that if you have recovered from COVID, and you have a healthy immune system, you will have developed immunity against reinfection. And this will protect you for at least 12 weeks. </p>
<p>As case numbers in Australia increase, the reports of reinfections are also on the rise. And it’s likely reinfection is occurring sooner than we first thought. </p>
<h2>What’s happening in our body?</h2>
<p>In order for a person to fight off re-infection with any virus, they must have developed a <a href="https://theconversation.com/how-long-does-protective-immunity-against-covid-19-last-after-infection-or-vaccination-two-immunologists-explain-177309">protective immune response</a>. </p>
<p>Two main factors decide whether a person will have a protective immune response:</p>
<p>1) how long a person’s immune memory lasts </p>
<p>2) how well that memory recognises the virus, or a slightly different virus. </p>
<p>Immune memory is made up of many critical parts, which each play a role in the protective army of your immunity. The biggest players in protective immunity memory are your B-cells (which mature to make antibodies) and your T-cells (which destroy virus-infected host cells).</p>
<p>So far, the evidence suggests immune memory for SARS-CoV-2, the virus that causes COVID, lasts for <a href="https://www.nature.com/articles/s41467-021-24979-9">months</a> or even <a href="https://www.frontiersin.org/articles/10.3389/fmed.2021.684864/full">years</a> when it comes to B-cells and the antibodies they produce. </p>
<p>Similarly, <a href="https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(22)00036-2/fulltext">current evidence</a> shows the memory T-cells can last over a year.</p>
<p>This means that for a healthy person, immune memory for SARS-CoV-2 appears to last for a year, against reinfection with the exact same virus. </p>
<figure class="align-center ">
<img alt="SARS-CoV-2 animation." src="https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=337&fit=crop&dpr=1 600w, https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=337&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=337&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/462657/original/file-20220512-16-gb6u6j.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=424&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">The immune memory from SARS-CoV-2 might last months or even years.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/sarscov2-coronavirus-virus-which-causes-covid19-1697804203">Shutterstock</a></span>
</figcaption>
</figure>
<h2>So why the reinfections?</h2>
<p>One clear explanation for reinfection is the virus is mutating. SARS-CoV-2 replicates fast and in doing so makes replication errors. We refer to these errors as mutations. Over time, the mutations accumulate and a new sub-variant is born. </p>
<p>Since the start of the pandemic we have seen the parental Wuhan strain mutate to Alpha, Beta, Delta and now Omicron. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-are-there-so-many-new-omicron-sub-variants-like-ba-4-and-ba-5-will-i-be-reinfected-is-the-virus-mutating-faster-182274">Why are there so many new Omicron sub-variants, like BA.4 and BA.5? Will I be reinfected? Is the virus mutating faster?</a>
</strong>
</em>
</p>
<hr>
<p>The current theory is that immunity from one variant may not provide enough protection from another. </p>
<p>Data so far suggest the Omicron variant is <a href="https://www.science.org/doi/10.1126/science.abn4947">better at immune escape</a> than its predecessors. This means Omicron is “escaping” the immune memory created by SARS-CoV-2 infections from other variants such as Delta, Beta or Alpha. </p>
<p>Emerging data is now showing sub-variants of Omicron can also escape immunity from a previous Omicron variant. This means a person might be able to get an Omicron reinfection. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1523425497127931904"}"></div></p>
<p>A small, yet to be peer-reviewed <a href="https://www.medrxiv.org/content/10.1101/2022.02.19.22271112v1.full">study from Denmark</a> found that in unvaccinated people, reinfection with Omicron BA.2 is possible following a primary infection with Omicron BA.1. Despite this finding, the study also concluded reinfection rates were low and therefore rare. </p>
<p>With winter approaching and case numbers climbing, we’re also <a href="https://www.smh.com.au/national/nsw/tens-of-thousands-of-covid-19-reinfections-likely-in-nsw-as-first-ba-4-case-detected-20220428-p5agta.html">seeing</a> the emergence of <a href="https://www.abc.net.au/news/2022-04-15/new-covid-omicron-variant-ba4-ba5-detected-australia/100994610#:%7E:text=The%20BA.4%20and%20BA.5%20subvariants%20have%20not%20been,from%20the%20Tullamarine%20catchment%20in%20the%20city%27s%20north-west">new sub-variants</a> such as BA.4 and BA.5. Early evidence <a href="https://www.biorxiv.org/content/10.1101/2022.04.30.489997v1">shows</a> these new sub-variants are even better at escaping immune memory than the parental BA.1 Omicron.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/ba-2-is-like-omicrons-sister-heres-what-we-know-about-it-so-far-176137">BA.2 is like Omicron's sister. Here's what we know about it so far</a>
</strong>
</em>
</p>
<hr>
<h2>What about severity?</h2>
<p>For those who get a reinfection, disease severity appears to be <a href="https://www.nejm.org/doi/full/10.1056/NEJMc2108120">milder</a> and less likely to result in hospitalisation. This is likely because the immune memory can recognise at least part of the re-infecting virus. </p>
<p>However it’s difficult to measure disease severity on a <a href="https://www.nature.com/articles/s41577-022-00720-5">population level</a>. A <a href="https://ghrp.biomedcentral.com/articles/10.1186/s41256-022-00245-3">systemic review</a> of case studies found that while some second infections were milder, this was not so in all cases. Some reinfections resulted in worse outcomes, including death. (During this study period, one of the <a href="https://cov-lineages.org/lineage_list.html">original strains</a>, B.1, caused most primary infections, with reinfections caused by Alpha or Beta variants.) </p>
<p>But while Omicron appears to be causing <a href="https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/coronaviruscovid19infectionsurveycharacteristicsofpeopletestingpositiveforcovid19uk/2february2022#reinfections-with-covid-19-uk">more reinfections</a> than other variants, there isn’t enough robust data to make firm conclusions about the <a href="https://www.tandfonline.com/doi/full/10.1080/22221751.2022.2052358">severity of reinfection</a> with Omicron or other variants. </p>
<p>What we know for certain is we need more data from more people to say that <a href="https://www.tandfonline.com/doi/full/10.1080/20009666.2021.1974665">reinfection is less severe</a>. </p>
<p>We also know from several studies that being vaccinated does provide <a href="https://www.nejm.org/doi/10.1056/NEJMoa2119497">protection from reinfection</a>, including in previously infected people who then receive subsequent vaccines. </p>
<figure class="align-center ">
<img alt="ICU clinicians treat a patient with COVID." src="https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/462660/original/file-20220512-15-qbk4ir.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Some reinfections cause severe illness.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/doctors-protective-suits-masks-intensive-care-1852547962">Shutterstock</a></span>
</figcaption>
</figure>
<h2>Another reason to get boosted</h2>
<p>A <a href="https://www.medrxiv.org/content/10.1101/2022.04.29.22274477v1">recent study</a> that’s yet to be peer-reviewed found immunity from Omicron BA.1 variant drops around 7.5 fold with the new Omicron BA.4 and BA.5 variants. This means the antibodies you produce from a BA.1 infection, which are able to detect and neutralise the BA.1 virus, are 7.5 times less able to recognise and neutralise BA.4 and BA.5 than BA.1. </p>
<p>This study also found vaccination plus natural exposure to Omicron BA.1 gave five times greater protection to Omicron BA.4 and BA.5 than the immunity from natural exposure to BA.1 alone. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/covid-reinfections-are-they-milder-and-do-they-strengthen-immunity-176592">COVID reinfections: are they milder and do they strengthen immunity?</a>
</strong>
</em>
</p>
<hr>
<p>Data <a href="https://www.medrxiv.org/content/10.1101/2022.03.22.22272745v1">also shows</a> the strongest protective immunity comes from a mix of triple vaccination and natural infection. </p>
<p>A further study <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(22)00143-8/fulltext">found</a> this type of hybrid immunity protects better against both reinfection and hospitalisation than natural immunity alone, highlighting the importance of vaccination and vaccine boosters. </p>
<p>So the question remains: if our immune memory lasts for a year, but is too specific to recognise the new variants, will we need a new vaccine every year? Time will tell.</p><img src="https://counter.theconversation.com/content/182154/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lara Herrero receives funding from NHMRC on emerging infectious diseases. </span></em></p>You know the symptoms because you’ve already had COVID once. So what can you expect when you’re reinfected? And why does it happen?Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1734902021-12-17T15:11:21Z2021-12-17T15:11:21ZCOVID: how the disease moves through the air<figure><img src="https://images.theconversation.com/files/437843/original/file-20211215-23-mvg91m.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/aerosols-corona-viruses-indoors-3d-illustration-1827265097">Alexander Limbach/shutterstock</a></span></figcaption></figure><p>Masks have been a common sight all over the world since SARS-CoV-2, the novel coronavirus, invaded our lives. We set out to investigate if they work. Our goal was to find out how the virus travels through the air in buildings so we could understand more about the risk of airborne infection – including whether masks can help to control the number of respiratory droplets in the air and therefore reduce transmission. </p>
<p>This is what we know so far.</p>
<p>As we talk, cough and breathe, a jet of air rushes out of our lungs through our mouth and nose – in the process, it gathers respiratory fluid from the lungs, throat, and mouth creating droplets which are then <a href="https://www.science.org/doi/10.1126/science.abd9149">emitted into the air</a>. High energy vocal activities, such as singing and coughing, <a href="https://www.tandfonline.com/doi/abs/10.1080/02786826.2021.1883544">increase the amount of droplets</a> and provide a greater force to propel these <a href="https://www.annualreviews.org/doi/10.1146/annurev-bioeng-111820-025044">further into the space</a> around us. </p>
<p>Most of the droplets produced are tiny at less than five microns (a micron is a thousandth of a millimetre) – <a href="https://doi.org/10.1016/j.jaerosci.2008.11.002">we call these aerosols</a>. Anything larger than this is called a droplet and these can be as large as <a href="https://www.sciencedirect.com/science/article/pii/S0021850208001882?via%3Dihub">100 microns</a>.</p>
<p>Each breath, word or cough will produce many thousands or millions of aerosols and droplets over a <a href="https://doi.org/10.1016/j.jaerosci.2008.11.002">spectrum of sizes</a>. Whatever their size, they are propelled forward in a <a href="https://jamanetwork.com/journals/jama/fullarticle/2763852/">cloud of warm humid air</a> from our mouth towards other people in a shared space. The larger droplets will tend to fall to the ground quickly due to gravity but smaller ones can remain suspended in the air for many hours.</p>
<p>Over the past 18 months, SARS-CoV-2 has been detected in air samples in many different situations, most often in places like hospitals. Generally, PCR tests were used to assess whether SARS-CoV-2 RNA was present. The viral RNA molecules were <a href="https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciab691/6343417">found in exhaled aerosols</a>, in numbers varying from the <a href="https://academic.oup.com/cid/article/73/7/e1870/5868534">10s</a> to the <a href="https://www.cambridge.org/core/journals/infection-control-and-hospital-epidemiology/article/air-and-environmental-sampling-for-sarscov2-around-hospitalized-patients-with-coronavirus-disease-2019-covid19/2603FF55AA16BB839ED5A500DF62EFAE">100,000s</a> per cubic metre of room air.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/omicron-and-covid-boosters-everything-you-need-to-know-173694">Omicron and COVID boosters: everything you need to know</a>
</strong>
</em>
</p>
<hr>
<h2>Infected people are the source</h2>
<p>We now know that asymptomatic infected people <a href="https://thorax.bmj.com/content/76/1/61">do not necessarily</a> have a lower viral load than those displaying symptoms. In both cases the amount of virus can be as little as a <a href="https://www.bmj.com/content/369/bmj.m1443">few thousand</a> or as many as <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30113-4/fulltext">hundreds of billions</a> of viral genomes in a millilitre of saliva or nose sputum, a proportion of which will be live virus. </p>
<p>Therefore, as a micron is a thousandth of a millimetre, we can work out that at the time when they leave the body there will probably be few virus particles in most aerosols of five microns – but there might be from tens to tens of thousands of virus particles in a 100-micron droplet. And each breath, word or cough will produce many thousands or millions of aerosols and droplets over a <a href="https://doi.org/10.1016/j.jaerosci.2008.11.002">spectrum of sizes</a>.</p>
<p>Once exposed to the drier air outside our body, <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/ina.12297?casa_token=8-Q6047L2ecAAAAA%3AafO38_8fZ7H9XRpwNwMZwPVIkkoQzoRDuLfYova3LFf97LfjZf5VaxnnAEsFWPcwKYF1lb7jJmBRmZzU">fluid evaporates from the virus-laden larger droplets</a> which then become aerosols – the number of virus particles remains the same, but they are concentrated into a much smaller and lighter aerosol. That means that they can stay suspended in the air for hours and pose an infection risk.</p>
<h2>The risk of indoor settings</h2>
<p>We know that in a given room the amount of virus someone inhales is <a href="https://www.sciencedirect.com/science/article/pii/S0360132321000305?via%3Dihub">directly proportional</a> to the amount of virus emitted into the air by an infected person. In simple terms, the more virus is breathed out into a room, the more other people in the room will breathe it in.</p>
<figure class="align-center ">
<img alt="Man wearing face mask using mobile phone on a plane" src="https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/438339/original/file-20211219-19-l6uojw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Wearing a face mask indoors can help to catch viral particles.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/man-wearing-face-mask-using-phone-1793748499">Jaromir Chalabala/shutterstock</a></span>
</figcaption>
</figure>
<p>The exact amount of virus a susceptible person inhales depends on several factors including <a href="https://doi.org/10.1016/j.scitotenv.2021.148749">proximity</a> to the infected person (or people) and time spent in the enclosed setting. The virus is more concentrated closer to the infected person, whereas at distances greater than two metres, the virus in the exhaled air will dissipate and become diluted within the room volume. But – and this is where the real danger lies – in poorly ventilated spaces the virus quantity can build up. So, if you spend longer in a room with virus laden air, you will <a href="https://www.sciencedirect.com/science/article/pii/S0360132321000305?via%3Dihub">inhale more virus</a>. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/a-year-of-covid-vaccines-how-the-uk-pinned-its-hopes-on-the-jab-and-why-those-hopes-are-under-threat-171274">A year of COVID vaccines: how the UK pinned its hopes on the jab – and why those hopes are under threat</a>
</strong>
</em>
</p>
<hr>
<h2>Masks catch viral particles</h2>
<p>It is <a href="https://www.bmj.com/content/375/bmj.n2729">challenging to exactly measure</a> the net benefit of masks on a population because of the vast <a href="https://elifesciences.org/articles/65774">variations in viral load</a> between people, whether they are singing, shouting or talking, the size of the indoor space and time spent in it. Masks make a relatively small difference when people release just a few viruses every hour because they were never releasing enough virus to infect another person. Likewise at the other end of the spectrum, reducing the emission from super-emitters still often results in high overall emission of virus. Wearing a mask will reduce the amount of virus emitted, but how much it helps is dependent on how much virus is being emitted in the first instance. </p>
<p>Therefore, there is <a href="https://www.bmj.com/content/375/bmj-2021-068302">no conclusive evidence</a> on their efficacy because it’s so hard to adjust for all the other variables which affect the level of transmission. </p>
<p>But even without certainty over the exact number of cases prevented by wearing a mask, we do know that they will <a href="https://www.sciencedirect.com/science/article/pii/S0163445321001353">definitely catch some of the virus</a> laden aerosols and droplets – and that <a href="https://www.gov.uk/government/publications/ukhsa-face-coverings-and-covid-19-statement-from-an-expert-panel-14-october-2021">will have</a> an <a href="https://www.gov.uk/government/publications/spi-b-spi-m-and-emg-considerations-for-potential-impact-of-plan-b-measures-13-october-2021">impact on reducing the number of infections</a>. </p>
<p>A mask is one of many weapons in our arsenal which also includes vaccination, social distancing, ventilation and hygiene. As the <a href="https://www.who.int/publications/m/item/weekly-epidemiological-update-on-covid-19---7-december-2021">omicron variant</a> rapidly spreads, the case numbers are very worrying. It is more important than ever that we use all the means we have available to reduce the spread of SARS-CoV-2.</p><img src="https://counter.theconversation.com/content/173490/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lena Ciric receives funding from UKRI. </span></em></p><p class="fine-print"><em><span>Abigail Hathway recieves funding from UKRI, Health and Safety Executive and Sheffield City Council. She is a member of the Chartered Institute of Building Services Engineers</span></em></p><p class="fine-print"><em><span>Benjamin Jones receives funding from the Engineering and Physical Sciences Research Council. He an affiliate of the Chartered Institution of Building Services Engineers.</span></em></p><p class="fine-print"><em><span>Chris Iddon receives funding from UKRI. He a member of the Chartered Institution of Building Services Engineers.</span></em></p>Masks definitely catch some of the virus laden aerosols and droplets - and that will reduce transmission between people and the number of cases of COVID-19.Lena Ciric, Associate Professor in Environmental Engineering, UCLAbigail Hathway, Senior lecturer, University of SheffieldBenjamin Jones, Associate Professor, Department of Architecture and Built Environment, University of NottinghamChris Iddon, Research associate, Built environment, University of NottinghamLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1720132021-11-22T16:27:00Z2021-11-22T16:27:00ZBird flu outbreaks in Europe: what you need to know<p>Once again, Europe is experiencing bird flu outbreaks – the deadliest animal disease known. In chickens and turkeys, <a href="https://www.sciencedirect.com/science/article/pii/S0378113500001607?via%3Dihub">over 90%</a> of an affected flock will die within a couple of weeks, although in ducks and geese the disease may be milder.</p>
<p>Bird flu outbreaks are caused by avian influenza viruses, most of which cause mild infection in birds, but two sub-types (called H5 and H7) can occur as a very deadly virus. </p>
<p>Flu viruses have a high mutation rate and can exchange genes when two viruses simultaneously infect a single host. These genetic changes allow them to change their make up and escape immunity in their host and continue spreading.</p>
<p>In the previous century, epidemics of the deadly bird flu were rare and always originated from mild H5 or H7 viruses that <a href="https://doc.oie.int/dyn/portal/digidoc.xhtml?statelessToken=IUK6OztgH_kivlL_Kka2fnPew1Nz3pbqBVGeS_9xDNE=&actionMethod=dyn%2Fportal%2Fdigidoc.xhtml%3AdownloadAttachment.openStateless">mutated into</a> a deadly virus while transmitting in a chicken or turkey flock. Until 1996, resulting outbreaks and epidemics were either effectively controlled or faded out due to a lack of susceptible hosts. </p>
<h2>H5N1 emerges</h2>
<p>Infections caused by these deadly viruses were also never seen in wild birds. This changed after the emergence of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787969/">the H5N1 virus</a> in China. Outbreaks in poultry were not effectively controlled. The virus gradually expanded its territory across China, and from 2003, further into Asia and Africa. Humans in close contact with infected poultry could become infected, resulting in the death of <a href="https://cdn.who.int/media/docs/default-source/influenza/human-animal-interface-risk-assessments/2021_aug_tableh5n1.pdf?sfvrsn=12194b1_6&download=true">456 people</a> to date.</p>
<p>Wild birds became infected because of a spillover from the ongoing spread of the virus in poultry. This gave rise to new H5 viruses that were still deadly to poultry, but of little harm to certain waterbird species. Consequently, migratory waterbirds could fly thousands of kilometres, despite being infected by these viruses, and so were able to spread the viruses over very large distances. </p>
<p>In 2005, wild waterbirds introduced the virus to Europe for the first time during fall migration. This was the first sign that the ecology of these viruses had completely changed; a virus strictly associated with poultry had adapted itself to wild water birds, tremendously increasing its survival potential.</p>
<p>Each year in spring and summer, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5972003/">waterbirds mingle</a> on their breeding grounds in Siberia and mix their influenza viruses, creating new variants they then bring to Europe, Asia and Africa during fall migration, causing deadly outbreaks in poultry.</p>
<p>Obviously, there is little we can do to control infections in the wild water birds. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7009867/">Surveillance is recommended</a> to assess the risk of virus exposure to poultry and the removal of carcasses of dead birds from the environment. </p>
<p>Poultry farmers in areas with many waterbirds that stay there over winter are advised to keep poultry inside and should implement biosecurity measures to keep the virus out of their sheds. Faeces of infected wild birds <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8048466/">can contain</a> high amounts of virus and can easily enter a poultry shed by uncleaned boots or materials.</p>
<p>Current biosecurity programmes have not been sufficiently effective to prevent infections in risk areas. In the season 2020-21 there were <a href="https://www.efsa.europa.eu/sites/default/files/2021-05/9989.pdf">over 1,000 outbreaks</a> in the EU alone. And in the current season, tens of outbreaks have already been detected. </p>
<p>The yearly recurring outbreaks, with the associated mass killing of poultry, are an obvious threat to the sustainability of poultry farming. </p>
<h2>Poultry vaccine</h2>
<p>Vaccination could be a tool to help solve the problem. However, it is forbidden in many countries and its use results in trade barriers for poultry. The reason for the trade barriers is that most current vaccines prevent disease, but <a href="https://www-sciencedirect-com.proxy.library.uu.nl/science/article/pii/S0034528814002501?via%3Dihub">don’t stop transmission</a> of the infection. </p>
<p>A vaccine that stops disease but doesn’t stop transmission will result in “silent” virus spread, which compromises outbreak control and is undesirable because the virus has the potential to spread from animals to humans. </p>
<p>Fortunately, most of the currently circulating H5 virus variants are <a href="https://www.who.int/docs/default-source/wpro---documents/emergency/surveillance/avian-influenza/ai-20211112.pdf?sfvrsn=30d65594_181">not as dangerous</a> to humans as their ancestor H5N1. Still, caution is needed as this could easily change because of the virus’s ability to change its genetic code. </p>
<p>We urgently need effective vaccines for poultry – it is the only sustainable solution. New-generation vaccines may have more potential to control bird flu, but their effectiveness to stop virus transmission <a href="https://www.internationalegg.com/app/uploads/2018/01/AI-Vaccination-Document-Final.pdf">should be demonstrated</a> in the field. Such vaccines will not only protect poultry but also minimise exposure of humans to the virus.</p><img src="https://counter.theconversation.com/content/172013/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Arjan Stegeman receives funding from Dutch ministry of Agriculture, Nature and food safety. </span></em></p>Each year in spring and summer, waterbirds mingle on their breeding grounds in Siberia and mix their flu viruses, creating new variants they then bring to Europe, Asia and Africa.Arjan Stegeman, Professor of Veterinary Medicine, Utrecht UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1691312021-10-19T12:23:41Z2021-10-19T12:23:41ZViruses are both the villains and heroes of life as we know it<figure><img src="https://images.theconversation.com/files/426749/original/file-20211015-16-1e3elye.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2380%2C1252&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Bacteriophages are viruses that infect bacteria and play a potential role in the evolution of life.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/bacteriophage-on-bacterium-illustration-royalty-free-illustration/1191008746"> NANOCLUSTERING/SCIENCE PHOTO LIBRARY/Science Photo Library via Getty Images</a></span></figcaption></figure><p>Viruses have a bad reputation. They are responsible for the COVID-19 pandemic and a <a href="https://viralzone.expasy.org/678">long list of maladies</a> that have plagued humanity since time immemorial. Is there anything to celebrate about them?</p>
<p>Many <a href="https://scholar.google.com/citations?user=T1I1sNAAAAAJ&hl=en">biologists like me</a> believe there is, at least for one specific type of virus – namely, <a href="https://www.ncbi.nlm.nih.gov/books/NBK493185/">bacteriophages</a>, or viruses that infect bacteria. When the DNA of these viruses is captured by a cell, it may contain instructions that enable that cell to perform new tricks.</p>
<h2>The mighty power of bacterial viruses</h2>
<p>Bacteriophages, or phages for short, keep bacterial populations in check, both on land and at sea. They kill <a href="https://dx.doi.org/10.1002%2Fbies.201400152">up to 40% of the oceans’ bacteria every day</a>, helping control <a href="https://doi.org/10.1111/j.1574-6976.2010.00258.x">bacterial blooms and redistribution of organic matter</a>.</p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/YI3tsmFsrOg?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Bacteriophages are viruses that kill specific types of bacteria.</span></figcaption>
</figure>
<p>Their ability to selectively kill bacteria also has medical doctors excited. Natural and engineered phages have been <a href="https://dx.doi.org/10.1038%2Fs41591-019-0437-z">successfully used to treat bacterial infections</a> that do not respond to antibiotics. This process, known as <a href="https://dx.doi.org/10.4292%2Fwjgpt.v8.i3.162">phage therapy</a>, could help fight <a href="https://dx.doi.org/10.1179%2F2047773215Y.0000000030">antibiotic resistance</a>.</p>
<p><a href="https://doi.org/10.1093/nar/gkab773">Recent research</a> points to another important function of phages: They may be nature’s ultimate genetic tinkerers, crafting novel genes that cells can retool to gain new functions.</p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Illustration of bacteriophage structure." src="https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=1014&fit=crop&dpr=1 600w, https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=1014&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=1014&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1274&fit=crop&dpr=1 754w, https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1274&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/426550/original/file-20211014-27-n6jugx.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1274&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Bacteriophage caspids can carry extra DNA that the virus can tinker with.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/flat-illustration-of-bacteriophage-royalty-free-illustration/1285360925">Kristina Dukart/iStock via Getty Images Plus</a></span>
</figcaption>
</figure>
<p>Phages are the most abundant life form on the planet, with <a href="https://dx.doi.org/10.1128%2FAEM.01465-08">a nonillion – that’s a 1 with 31 zeroes after it – of them floating around the world</a> at any moment. Like all viruses, phages also have <a href="https://doi.org/10.1128/JVI.00694-10">high replication and mutation rates</a>, meaning they form many variants with different characteristics each time they reproduce.</p>
<p>Most phages have a <a href="https://dx.doi.org/10.1007%2Fs00018-007-6451-1">rigid shell called a capsid</a> that is filled with their genetic material. In many cases, the shell has more space than the phage needs to store the DNA essential for its replication. This means that phages have room to carry extra genetic baggage: genes that are not actually necessary for the phage’s survival that it can modify at will.</p>
<h2>How bacteria retooled a viral switch</h2>
<p>To see how this plays out, let’s take a deeper look at the phage life cycle.</p>
<p>Phages come in two main flavors: temperate and virulent. <a href="https://dx.doi.org/10.1038%2Fismej.2017.16">Virulent phages</a>, like many other viruses, operate on an invade-replicate-kill program. They enter the cell, hijack its components, make copies of themselves and burst out.</p>
<p><a href="https://dx.doi.org/10.1038%2Fismej.2017.16">Temperate phages</a>, on the other hand, play the long game. They fuse their DNA with the cell’s and may lay dormant for years until something triggers their activation. Then they revert to virulent behavior: replicate and burst out. </p>
<p>Many temperate phages use DNA damage as their trigger. It’s sort of a “Houston, we have a problem” signal. If the cell’s DNA is being damaged, that means the DNA of the resident phage is likely to go next, so the phage wisely decides to jump ship. The genes that direct phages to replicate and burst out are turned off unless DNA damage is detected.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram of lytic and lysogenic cycles of bacteriophages." src="https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=423&fit=crop&dpr=1 600w, https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=423&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=423&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=531&fit=crop&dpr=1 754w, https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=531&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/426559/original/file-20211014-19-1g3475j.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=531&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Virulent phages follow the lytic cycle of viral reproduction, destroying their hosts as soon as they complete replication. Temperate phages, on the other hand, follow the lysogenic cycle and stay dormant inside their host’s DNA until they’re triggered to burst out.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Figure_21_02_03.png">CNX OpenStax/Wikimedia Commons</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>Bacteria have retooled the mechanisms controlling that life cycle to generate a complex genetic system that my collaborators and I have been <a href="https://erilllab.umbc.edu/">studying for over two decades</a>.</p>
<p>[<em>Research into coronavirus and other news from science</em> <a href="https://theconversation.com/us/newsletters/science-editors-picks-71/?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=science-corona-research">Subscribe to The Conversation’s new science newsletter</a>.]</p>
<p>Bacterial cells are also interested in knowing if their DNA is getting busted. If it is, they activate a set of genes that attempt to repair the DNA. This is known as the <a href="https://doi.org/10.1111/j.1574-6976.2007.00082.x">bacterial SOS response</a> because, if it fails, the cell is toast. Bacteria orchestrate the SOS response using a switch-like protein that responds to DNA damage: It turns on if there is damage and stays off if there isn’t. </p>
<p>Perhaps not surprisingly, bacterial and phage switches are evolutionarily related. This prompts the question: Who invented the switch, bacteria or viruses?</p>
<p>Our previous research and <a href="https://doi.org/10.1046/j.1365-2958.2003.03713.x">work by other researchers</a> indicates that phages got there first. In our <a href="https://doi.org/10.1093/nar/gkab773">recent report</a>, we discovered that the SOS response of <em>Bacteroidetes</em>, a group of bacteria that <a href="https://dx.doi.org/10.3390%2Fnu12051474">comprise up to a half of the bacteria living in your gut</a>, is under control of a phage switch that was retooled to implement the bacteria’s own complex genetic programs. This suggests that bacterial SOS switches are in fact phage switches that got retooled eons ago.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram of bacterial genetic switch capture process." src="https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=394&fit=crop&dpr=1 600w, https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=394&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=394&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=495&fit=crop&dpr=1 754w, https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=495&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/426739/original/file-20211015-57123-3pn3x.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=495&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">When a temperate phage infects a bacterial cell and integrates its genome with the cell’s DNA, it typically lays dormant until it’s triggered to burst out of the cell. But once the phage’s DNA is part of the bacterium’s, mutations can disrupt the phage’s genetic material and render it inactive. This means that when DNA damage occurs, the phage won’t be able to reform itself and burst out. Over time, the bacterium may adapt the phage’s switch to control its own SOS response genes.</span>
<span class="attribution"><a class="source" href="https://doi.org/10.1093/nar/gkab773">Miquel Sánchez-Osuna/Created with BioRender.com</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-nd/4.0/">CC BY-NC-ND</a></span>
</figcaption>
</figure>
<p>It’s not just bacterial switches that appear to be phage inventions. Beautiful detective work has shown that a bacterial gene needed for cell division also arose through <a href="https://dx.doi.org/10.1016%2Fj.cub.2019.04.032">“domestication” of a phage toxin gene</a>. And many bacterial attack systems, such as <a href="https://doi.org/10.2217/fmb.11.124">toxins</a> and the <a href="https://dx.doi.org/10.1128%2FMMBR.00014-11">genetic guns</a> used to inject them into cells, as well as the <a href="https://dx.doi.org/10.1128%2FMMBR.68.3.560-602.2004">camouflage</a> they use to evade the immune system, are known or suspected to have phage origins. </p>
<h2>The upside of viruses</h2>
<p>OK, you may think, phages are great, but the viruses that infect us are certainly not cool. Yet there is mounting evidence that the viruses that infect plants and animals are also a major source of genetic innovation in these organisms. Domesticated viral genes have been shown, for instance, to play a key role in the <a href="https://dx.doi.org/10.3389%2Ffmicb.2012.00262">evolution of mammalian placentas and in keeping human skin moist</a>.</p>
<p>Recent evidence suggests that even the <a href="https://doi.org/10.3389/fmicb.2020.571831">nucleus of a cell, which houses DNA, could have also been a viral invention</a>. Researchers have also speculated that the ancestors of today’s viruses may have pioneered <a href="https://dx.doi.org/10.1098%2Frstb.2015.0442">the use of DNA as the primary molecule for life</a>. Not a small feat.</p>
<p>So while you may be used to thinking of viruses as the quintessential villains, they are arguably nature’s powerhouses for genetic innovation. Humans are likely here today because of them.</p><img src="https://counter.theconversation.com/content/169131/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ivan Erill receives funding from the US National Science Foundation</span></em></p>Viruses have gotten a bad rap for the many illnesses and pandemics they’ve caused. But viruses are also genetic innovators – and possibly the pioneers of using DNA as the genetic blueprint of life.Ivan Erill, Associate Professor of Biological Sciences, University of Maryland, Baltimore CountyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1655382021-09-28T20:13:20Z2021-09-28T20:13:20ZHow contagious is Delta? How long are you infectious? Is it more deadly? A quick guide to the latest science<figure><img src="https://images.theconversation.com/files/422542/original/file-20210922-23-68rivz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-woman-face-mask-using-mobile-1685691625">Shutterstock</a></span></figcaption></figure><p>Delta was recognised as a SARS-CoV-2 <a href="https://www.cdc.gov/coronavirus/2019-ncov/variants/variant-info.html#anchor_1632154493691">variant of concern</a> in <a href="https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/">May 2021</a> and has proved extremely difficult to control in unvaccinated populations. </p>
<p>Delta has managed to <a href="https://medicalxpress.com/news/2021-09-delta-overwhelming-covid-variants.html">out-compete</a> other variants, including Alpha. Variants are classified as “of concern” because they’re either more contagious than the original, cause more hospitalisations and deaths, or are better at evading vaccines and therapies. Or all of the above. </p>
<p>So how does Delta fare on these measures? And what have we learnt since Delta was first listed as a variant of concern?</p>
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Read more:
<a href="https://theconversation.com/is-delta-defeating-us-heres-why-the-variant-makes-contact-tracing-so-much-harder-164780">Is Delta defeating us? Here's why the variant makes contact tracing so much harder</a>
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<h2>How contagious is Delta?</h2>
<p>The R0 tells us how many other people, on average, one infected person will pass the virus on to. </p>
<p>Delta has an <a href="https://www.bbc.com/news/health-57431420">R0 of 5-8</a>, meaning one infected person passes it onto five to eight others, on average.</p>
<p>This compares with an R0 of 1.5-3 for the original strain. </p>
<p>So Delta is twice to five times as contagious as the virus that circulated in 2020. </p>
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<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=1023&fit=crop&dpr=1 600w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=1023&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=1023&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1285&fit=crop&dpr=1 754w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1285&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1285&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"></span>
<span class="attribution"><span class="source">The Conversation</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<hr>
<h2>What happens when you’re exposed to Delta?</h2>
<p>SARS-CoV-2 is the virus that causes COVID-19. SARS-CoV-2 is transmitted through droplets an infected person releases when they breathe, cough or sneeze. </p>
<p>In some circumstances, transmission also occurs when a person touches a contaminated object, then touches their face. </p>
<figure class="align-center ">
<img alt="Four Turkish men walk across an open town space." src="https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">One person infected with Delta infects, on average, five to eight others.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/turkey-03-20-2020-four-people-1678223533">Shutterstock</a></span>
</figcaption>
</figure>
<p>Once SARS-CoV-2 enters your body – usually through your nose or mouth – it starts to replicate. </p>
<p>The period from exposure to the virus being detectable by a PCR test is called the <em>latent</em> period. For Delta, one study suggests this is an <a href="https://www.medrxiv.org/content/10.1101/2021.07.07.21260122v2">average of four days</a> (with a range of three to five days). </p>
<p>That’s two days faster than the original strain, which took roughly six days (with a range of five to eight days). </p>
<hr>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=761&fit=crop&dpr=1 600w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=761&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=761&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=957&fit=crop&dpr=1 754w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=957&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=957&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"></span>
<span class="attribution"><span class="source">The Conversation</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<hr>
<p>The virus then continues to replicate. Although often there are no symptoms yet, the person has become infectious. </p>
<p>People with COVID-19 <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2783099">appear to be</a> most infectious two days before to three days after symptoms start, though it’s unclear whether this differs with Delta. </p>
<p>The time from virus exposure to symptoms is called the <em>incubation</em> period. But there is often a gap between when a person becomes infectious to others to when they show symptoms. </p>
<p>As the virus replicates, the viral load increases. For Delta, the viral load is up to <a href="https://www.nature.com/articles/d41586-021-01986-w">roughly 1,200 times higher</a> than the original strain.</p>
<p>With faster replication and higher viral loads it is easy to see why Delta is challenging contact tracers and spreading so rapidly.</p>
<h2>What are the possible complications?</h2>
<p>Like the original strain, the Delta variant can affect many of the body’s organs including the lungs, heart and kidneys. </p>
<p>Complications include blood clots, which at their most severe <a href="https://www.abc.net.au/news/2021-08-07/delta-variant-of-covid-19-causing-heart-problems-young-people/100352868">can result in strokes or heart attacks</a>. </p>
<p>Around 10-30% of people with COVID-19 will experience prolonged symptoms, known as <a href="https://theconversation.com/the-mystery-of-long-covid-up-to-1-in-3-people-who-catch-the-virus-suffer-for-months-heres-what-we-know-so-far-161174">long COVID</a>, which can last for months and cause significant impairment, including in people who were previously well.</p>
<figure class="align-center ">
<img alt="Woman in a mask waits in hospital waiting room." src="https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Even previously well people can get long COVID.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/coronavirus-hospital-covid-19-woman-medical-1721906755">Shutterstock</a></span>
</figcaption>
</figure>
<p>Longer-lasting symptoms can include fatigue, shortness of breath, chest pain, heart palpitations, headaches, brain fog, muscle aches, sleep disturbance, depression and the loss of smell and taste.</p>
<h2>Is it more deadly?</h2>
<p>Evidence the Delta variant makes people sicker than the original virus is growing. </p>
<p>Preliminary studies from <a href="https://www.medrxiv.org/content/10.1101/2021.07.05.21260050v2">Canada</a> and <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3861566">Singapore</a> found people infected with Delta were more likely to require hospitalisation and were at greater risk of dying than those with the original virus. </p>
<p>In the Canadian study, Delta resulted in a 6.1% chance of hospitalisation and a 1.6% chance of ICU admission. This compared with other variants of concern which landed 5.4% of people in hospital and 1.2% in intensive care.</p>
<p>In the Singapore study, patients with Delta had a 49% chance of developing pneumonia and a 28% chance of needing extra oxygen. This compared with a 38% chance of developing pneumonia and 11% needing oxygen with the original strain. </p>
<p>Similarly, a published study from <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01358-1/fulltext">Scotland</a> found Delta doubled the risk of hospitalisation compared to the Alpha variant. </p>
<figure class="align-center ">
<img alt="Older man with cold symptoms lays down, wrapped in a blanket, cradling his head, holding a tissue to his nose." src="https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=401&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=401&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=401&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Emerging evidence suggests Delta is more likely to cause severe disease than the original strain.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/coronavirus-warning-old-people-senior-man-1505023982">Shutterstock</a></span>
</figcaption>
</figure>
<h2>How do the vaccines stack up against Delta?</h2>
<p>So far, the <a href="https://www.medrxiv.org/content/10.1101/2021.08.06.21261707v1.full.pdf">data show</a> a complete course of the <a href="https://www.nejm.org/doi/full/10.1056/nejmoa2108891">Pfizer</a>, <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3777268">AstraZeneca</a> or <a href="https://www.medrxiv.org/content/10.1101/2021.08.06.21261707v1.full.pdf">Moderna</a> vaccine reduces your chance of severe disease (requiring hospitalisation) by more than 85%. </p>
<p>While protection is lower for Delta than the original strain, studies show good coverage for all vaccines after two doses. </p>
<h2>Can you still get COVID after being vaccinated?</h2>
<p>Yes. <a href="https://theconversation.com/why-are-we-seeing-more-covid-cases-in-fully-vaccinated-people-an-expert-explains-166741">Breakthrough</a> infection occurs when a vaccinated person tests positive for SARS-Cov-2, regardless of whether they have symptoms. </p>
<p>Breakthrough infection <a href="https://theconversation.com/what-is-a-breakthrough-infection-6-questions-answered-about-catching-covid-19-after-vaccination-164909">appears more common</a> with Delta than the original strains.</p>
<p>Most symptoms of breakthrough infection <a href="https://theconversation.com/yes-you-can-still-get-covid-after-being-vaccinated-but-youre-unlikely-to-get-as-sick-163870">are mild</a> and don’t last as long. </p>
<p>It’s <a href="https://www.bbc.com/news/health-52446965#:%7E:text=Researchers%20conclude%20reinfection%20is%20uncommon,have%20had%20antibodies%20or%20not.">also possible</a> to get COVID twice, though this isn’t common. </p>
<h2>How likely are you to die from COVID-19?</h2>
<p>In Australia, over the life of the pandemic, 1.4% of people with COVID-19 have died from it, compared with 1.6% in the United States and 1.8% in the United Kingdom. </p>
<p>Data from the United States <a href="https://www.cdc.gov/mmwr/volumes/70/wr/mm7037e1.htm?s_cid=mm7037e1_w#T1_down">shows</a> people who were vaccinated were ten times less likely than those who weren’t to die from the virus. </p>
<p>The Delta variant is currently proving to be a challenge to control on a global scale, but with full vaccination and maintaining our social distancing practices, we reduce the spread. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-is-delta-such-a-worry-its-more-infectious-probably-causes-more-severe-disease-and-challenges-our-vaccines-163579">Why is Delta such a worry? It's more infectious, probably causes more severe disease, and challenges our vaccines</a>
</strong>
</em>
</p>
<hr>
<img src="https://counter.theconversation.com/content/165538/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lara Herrero does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Delta is more contagious and appears to be more deadly. And it’s more likely to land those infected in hospital and intensive care. Here’s what the latest evidence says about the dominant variant.Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1668192021-09-23T02:14:31Z2021-09-23T02:14:31ZCOVID-19 increases the chance of getting an autoimmune condition. Here’s what the science says so far<figure><img src="https://images.theconversation.com/files/422301/original/file-20210921-13-d1dkt8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/woman-unable-get-out-car-this-2020674380">Shutterstock</a></span></figcaption></figure><p>SARS-CoV-2, the virus that causes COVID-19, can sometimes cause the immune system to mistakenly attack the person’s own body. This process, known as “autoimmunity”, can damage a number of different organs. </p>
<p>After COVID-19, a small number of patients <a href="https://www.mdpi.com/1422-0067/22/16/8965/htm">have developed</a> a range of different autoimmune diseases. This includes <a href="https://www.nejm.org/doi/full/10.1056/NEJMc2009191">Guillain-Barré syndrome</a>, a disorder in which the immune system attacks nerves, often resulting in tingling and weakness in arms and legs. </p>
<p>There are also reports of autoimmune responses that don’t clearly correspond to any known autoimmune disease. This suggests COVID-19 disease may trigger new autoimmune illnesses. </p>
<p>The science on how and how often this occurs is still emerging. But here’s what we know so far. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-what-are-autoimmune-diseases-22577">Explainer: what are autoimmune diseases?</a>
</strong>
</em>
</p>
<hr>
<h2>First, a quick recap on the immune system</h2>
<p>The immune system is tightly regulated. Within it, immune cells known as B and T lymphocytes – the soldiers of the immune system – are normally able to distinguish between itself versus external targets. </p>
<p>When the system becomes confused, B and T cells may start to target our own bodies, which we call autoimmunity. </p>
<p>Viral infection can sometimes trigger this confusion, <a href="https://pubmed.ncbi.nlm.nih.gov/31430946/">resulting in autoimmune diseases</a>.</p>
<h2>How do viruses trigger autoimmunity?</h2>
<p>Two of the key mechanisms are “molecular mimicry” and “bystander activation”. </p>
<p>Molecular mimicry occurs when the part of the virus the B or T cells recognise looks similar to a normal protein in our body. </p>
<p>The B or T cell then sees both the viral and the self-protein as something to attack and eliminate. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-what-is-the-immune-system-19240">Explainer: what is the immune system?</a>
</strong>
</em>
</p>
<hr>
<p>Viral infections can also cause organ damage and cell death directly. When our cells die and burst, they release self-proteins. These would normally stay hidden and wouldn’t trigger an immune reaction. </p>
<p>Bystander activation occurs when B and T cells accidentally get in contact with self-proteins, confusing the immune system, which otherwise is trained to ignore self-proteins. </p>
<h2>What autoimmune conditions can COVID-19 trigger?</h2>
<p>There are <a href="https://www.mdpi.com/1422-0067/22/16/8965">multiple reports</a> of antibodies which recognise self-proteins, also known as autoantibodies, emerging in people with severe COVID-19.</p>
<p>Some of these autoantibodies that emerge in people with severe COVID recognise autoantibodies associated with <a href="https://www.mdpi.com/1422-0067/22/16/8965">well-known autoimmune diseases</a>, including:</p>
<ul>
<li><p><a href="https://jmedicalcasereports.biomedcentral.com/articles/10.1186/s13256-020-02582-8">systemic lupus erythematosus</a> (SLE), which affects joints, skin, blood cells as well as organs such as the brain, lungs and kidneys </p></li>
<li><p><a href="https://ard.bmj.com/content/early/2021/04/26/annrheumdis-2021-220479">rheumatoid arthritis</a>, affecting the joints</p></li>
<li><p><a href="https://onlinelibrary.wiley.com/doi/10.1111/jns.12419">Guillain-Barré syndrome</a>, mentioned above</p></li>
<li><p><a href="https://pubmed.ncbi.nlm.nih.gov/32420612/">immune thrombocytopenia</a>, which attacks blood platelets, resulting in excessive bruising and bleeding</p></li>
<li><p><a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7267601/">autoimmune haemolytic anaemia</a>, which attacks red blood cells which can result in breathlessness, tiredness, headaches and chest pain.</p></li>
</ul>
<figure class="align-center ">
<img alt="Close up of a person's had pushing their wheelchair." src="https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422518/original/file-20210922-21-1to343i.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Autoimmune conditions after COVID can affect the joints.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-woman-sitting-wheelchair-556849906">Shutterstock</a></span>
</figcaption>
</figure>
<p>In the reports that describe the onset of these diseases after COVID-19, the autoimmune symptoms start during or after the respiratory symptoms.</p>
<p>It’s unclear whether the patients were already predisposed to these diseases, or the infection unmasked an autoimmune process that had already begun. Or perhaps the infection triggered completely new autoimmunity. The triggers may even vary for different people. </p>
<p>COVID-19 may also trigger new autoimmune responses and, potentially, new autoimmune diseases. This has already occurred with a condition called multi-system inflammatory syndrome in children (MIS-C). </p>
<p>Originally described as a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7204765/">Kawasaki-like disease</a> associated with COVID-19, MISC-C causes <a href="https://www.who.int/news-room/commentaries/detail/multisystem-inflammatory-syndrome-in-children-and-adolescents-with-covid-19">additional symptoms</a> in children and adolescents with the condition. This includes rashes, shock, excessive bleeding, heart problems, and severe gastrointestinal symptoms. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/mis-c-is-a-rare-but-dangerous-illness-striking-children-weeks-after-they-get-covid-19-heres-what-we-know-about-it-145673">MIS-C is a rare but dangerous illness striking children weeks after they get COVID-19 – here's what we know about it</a>
</strong>
</em>
</p>
<hr>
<p>Autoantibodies measured in children diagnosed with MIS-C <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489877/">have a large variety of targets</a>. Many have no association to known autoimmune diseases, and instead are associated with the heart and surrounding tissue, as well as the gastrointestinal tract. </p>
<p>This indicates a potential mechanism for new autoimmune conditions that affect these organs.</p>
<h2>What’s causing the damage?</h2>
<p>Using computer-based prediction programs we <a href="https://www.frontiersin.org/articles/10.3389/fbinf.2021.709533/full">recently identified</a> regions of SARS-CoV-2 proteins that antibodies are likely to recognise and bind to. </p>
<p>We then compared them to all human proteins in the body, to identify potential similarities.</p>
<p>In doing so we were able to map the potential for SARS-CoV-2 infection to trigger autoantibody formation and existing or new autoimmune diseases, affecting different parts of the body. </p>
<p>Many of the human proteins we identified were associated with other diseases, including multiple sclerosis, SLE and rheumatoid arthritis.</p>
<p>Other human proteins we identified were associated with diseases of the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102662/">heart and vascular system</a>, <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30183-5/fulltext">airways</a>, as well as <a href="https://pubmed.ncbi.nlm.nih.gov/33315693/">epilepsy</a>, all of which have been reported in COVID-19 patients. </p>
<figure class="align-center ">
<img alt="Woman in a mask holds her chest above her heart." src="https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422519/original/file-20210922-17-1muao9e.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Emerging evidence suggests autoimmune conditions after COVID may also affect the heart.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/female-patient-wearing-mask-have-heart-2018442626">Shutterstock</a></span>
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<p>Currently much of our work is driven by computer-based predictive work; future laboratory research is needed to confirm the results.</p>
<p>Ultimately, understanding the mechanisms, the immune system targets, and those who are at risk, may offer targeted treatments for autoimmune illnesses after COVID-19.</p>
<h2>Could vaccination help?</h2>
<p>It’s unclear if getting vaccinated reduces your likelihood of getting these autoimmune conditions. </p>
<p>Autoantibodies have mainly been found after severe disease – and vaccination decreases disease severity. </p>
<p>So vaccination could reduce the risk of autoimmune symptoms after COVID-19, but at this stage it’s just speculative. </p>
<h2>What’s next for research in this area?</h2>
<p>Most reports of autoimmune disease after COVID-19 studied small patient numbers or are <a href="https://www.mdpi.com/1422-0067/22/16/8965">case reports</a>. Large studies reviewing the evidence are needed, especially covering multiple autoimmune diseases. </p>
<p>In one study, for example, five cases of Guillain-Barré Syndrome <a href="https://www.nejm.org/doi/full/10.1056/NEJMc2009191">were reported</a> out of 1,000-1,200 cases of COVID-19 admitted to the hospital. Although this indicates a small incidence in the autoimmune disease after COVID, it doesn’t tell us what is occurring worldwide. </p>
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Read more:
<a href="https://theconversation.com/an-autoimmune-like-antibody-response-is-linked-with-severe-covid-19-146255">An autoimmune-like antibody response is linked with severe COVID-19</a>
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<p><a href="https://ascpt.onlinelibrary.wiley.com/doi/10.1111/cts.12805">Reports</a> of the <a href="https://pubmed.ncbi.nlm.nih.gov/32581086/">percentage of people</a> positive for <a href="https://stm.sciencemag.org/content/12/570/eabd3876">autoantibodies to specific targets</a> range from 5% to a massive 50% in COVID-19 positive cases. </p>
<p>But although autoantibodies are <a href="https://www.science.org/doi/10.1126/science.abd4585">frequently found</a> in severe COVID cases, the precise role they play in illness after COVID remains unknown, with further studies required.</p><img src="https://counter.theconversation.com/content/166819/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>It’s unclear whether the patients were already predisposed to these diseases, or the infection unmasked a process that had already begun. Or perhaps the infection triggered a completely new illness.Magdalena Plebanski, Professor of Immunology, RMIT UniversityRhiane Moody, PhD candidate in immunology, RMIT UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1671052021-09-01T06:18:01Z2021-09-01T06:18:01ZThere’s no need to panic about the new C.1.2 variant found in South Africa, according to a virologist<figure><img src="https://images.theconversation.com/files/418789/original/file-20210901-27-b5a3f.jpg?ixlib=rb-1.1.0&rect=8%2C8%2C5982%2C3359&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/covid19-coronavirus-that-causes-respiratory-infections-1649506930">Shutterstock</a></span></figcaption></figure><p>Scientists in South Africa have discovered <a href="https://www.medrxiv.org/content/10.1101/2021.08.20.21262342v2.full">a new viral variant</a> of SARS-CoV-2, the virus that causes COVID-19.</p>
<p>It’s not a single virus but a clustering of genetically similar viruses, known as C.1.2.</p>
<p>The researchers, in a pre-print study released last week but yet to be peer reviewed, found this cluster has <a href="https://www.medrxiv.org/content/10.1101/2021.08.20.21262342v2.full">picked up a lot of mutations</a> in a short period of time. </p>
<p>Indeed, this is what viruses do. They continually evolve and mutate due to selective pressures but also because of opportunity, luck and chance.</p>
<p>C.1.2 has some concerning individual mutations. But we don’t really know how they’ll work together as a package. And it’s too early to tell how these variants will affect humans compared with other variants.</p>
<p>There’s no need to panic. It’s not spreading widely, and it’s not at Australia’s doorstep. The tools we have in place work against SARS-CoV-2, whatever the variant.</p>
<h2>Will it be more infectious or severe?</h2>
<p>C.1.2 is distinct from but on a genetic branch near the <a href="https://theconversation.com/the-lambda-variant-is-it-more-infectious-and-can-it-escape-vaccines-a-virologist-explains-164156">Lambda variant</a>, which is common in Peru.</p>
<p>It has some concerning individual mutations. But we don’t know how these mutations will work altogether, and we can’t predict how bad a variant will be based on mutations alone.</p>
<p>We need to see how a certain variant works in humans to give us an idea of whether it’s more transmissible, causes more severe disease or escapes the immunity we get from vaccines more than other variants.</p>
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<p>At this stage we don’t know enough about how C.1.2 behaves in humans because it hasn’t spread enough yet. It represents less than 5% of new cases in South Africa, and has only been found in around 100 COVID cases worldwide since May.</p>
<p>It’s not yet listed by the World Health Organization as a variant of interest or a variant of concern.</p>
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Read more:
<a href="https://theconversation.com/the-lambda-variant-is-it-more-infectious-and-can-it-escape-vaccines-a-virologist-explains-164156">The Lambda variant: is it more infectious, and can it escape vaccines? A virologist explains</a>
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<h2>Will it overtake other variants?</h2>
<p>It’s early days, so it’s impossible to predict what will happen to C.1.2.</p>
<p>It could expand and overtake other variants, or it could fizzle and disappear. </p>
<p>Again, just because this virus has a bunch of mutations, it doesn’t necessarily mean the mutations will work together to out-compete other variants.</p>
<p>Delta is the kingpin variant at the moment, so we need to keep an eye on C.1.2 to see if it starts to push out Delta.</p>
<p>So, it’s important to keep watching it in case it starts transmitting widely. One group in Australia, the Communicable Diseases Genomics Network, <a href="https://www.cdgn.org.au/">monitors these developments closely</a>.</p>
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Read more:
<a href="https://theconversation.com/why-is-delta-such-a-worry-its-more-infectious-probably-causes-more-severe-disease-and-challenges-our-vaccines-163579">Why is Delta such a worry? It's more infectious, probably causes more severe disease, and challenges our vaccines</a>
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<h2>There’s no need to panic</h2>
<p>At this point, there’s no need for concern.</p>
<p>Australia still has its border restrictions in place, so the odds of this rarely occurring virus coming into the country and spreading are very low.</p>
<p>There’s no evidence our vaccines don’t work against it. Our vaccines provide protection from severe disease and death against all other SARS-CoV-2 variants thus far and there’s a good chance they’ll continue to do so against C.1.2 variants.</p>
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Read more:
<a href="https://theconversation.com/whats-the-difference-between-mutations-variants-and-strains-a-guide-to-covid-terminology-154825">What's the difference between mutations, variants and strains? A guide to COVID terminology</a>
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<p>It won’t be long until we have a better idea of how C.1.2 behaves. There’s a lot of eyes on it, and we need to have patience as the data comes in.</p>
<p>Sensationalism and panic in the meantime isn’t going to solve anything.</p>
<p>New variants, and other bits of news amid the pandemic, are often latched onto and amplified by certain people and media. There’s a real risk this causes fear when it’s not needed, and inducing fear is a form of harm.</p>
<p>It is a tough time for the public because it’s hard to know who to listen to and trust.</p>
<p>I would say it’s best to listen to the experts, particularly organisations whose job it is to track and communicate risks about these things, like the WHO and your local jurisdiction’s health department.</p>
<p>Don’t amplify or pay attention to obvious alarmism and extreme negativity, and make sure you’re getting your information from media sources that are trustworthy.</p>
<h2>Vaccination remains our best single tool</h2>
<p>The chances of new variants arising increases the more the virus spreads.</p>
<p>Vaccinating as many people as possible, as quickly as possible, is key to reducing the risk of new variants arising.</p>
<p>That’s not to say it will reduce the risk to zero and there will be no more variants. Mutations happen by chance, and happen in a single person. One way mutations can arise is in people whose immune systems are compromised — they mount an incomplete immune response and the virus adapts, escapes and is released with more mutations.</p>
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<p>Nothing is perfect in biology. People’s immune systems respond in different ways, and a lot is based on individals’ immune history — how competent their immune system is and whether they have chronic disease.</p>
<p>We also won’t have every single person fully vaccinated, and vaccines aren’t 100% perfect, so there will still be some spread of the virus. </p>
<p>But vaccination reduces the risk a lot. We also know <a href="https://twitter.com/MackayIM/status/1432664147070578699">what else works to limit this virus</a>, including ventilation, filtering air, masks and social distancing measures.</p><img src="https://counter.theconversation.com/content/167105/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ian Mackay has previously received research funding from NHMRC and the ARC. </span></em></p>It’s not spreading widely, and it’s not at Australia’s doorstep. The tools we have in place work against the coronavirus.Ian M. Mackay, Adjunct Associate Professor, Faculty of Medicine, The University of QueenslandLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1661992021-08-19T13:39:56Z2021-08-19T13:39:56ZDavid Olufemi Olaleye: erudite virologist, excellent mentor and academic giant<figure><img src="https://images.theconversation.com/files/416535/original/file-20210817-27-12elf86.png?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">David Olufemi Olaleye </span> <span class="attribution"><span class="source">Courtesy African Digital Health Library</span></span></figcaption></figure><p>David Olufemi Olaleye, who passed away in <a href="https://www.vanguardngr.com/2021/07/makinde-mourns-top-ui-virologist-professor-olaleye/">July</a>, made an impact on many lives. He was an excellent teacher and mentor – like a father to many. A defender of the oppressed and a forthright person, who stood for the truth. </p>
<p>He was a researcher par excellence, highly knowledgeable, intelligent and humble. He supervised my master’s project in 1993 and I was his first PhD student. I worked closely with him for almost 30 years and it’s been difficult to accept that he is no more.</p>
<p>Olaleye was born on 21 July 1954 in Ogbomoso, southwest Nigeria. He obtained his Doctor of Veterinary Medicine in 1981, Master’s in Veterinary Science (Diagnostic Pathology) in 1983 and PhD in Virology in 1991, all from the University of Ibadan. He joined the university immediately after the mandatory one year national service in 1982 as Resident Veterinary Officer (Pathology). His journey as a virologist started when he was appointed lecturer in the Department of Virology, College of Medicine of the same university in 1986. He rose through the ranks and became Professor of Virology in 1995. He was appointed <a href="https://www.com.ui.edu.ng/index.php/the-college-of-medicine-university-of-ibadan-mourns-the-loss-of-professor-olufemi-david-olaleye">Consultant Virologist</a>, University College Hospital, Ibadan, Nigeria on 11 March 1992 and held this position as specialist adviser until his death.</p>
<p>He was also an Adjunct Professor at Northwestern University, Chicago, Illinois, USA. He was a founding member of the <a href="https://afrehealth.org/about/about-afrehealth">African Forum for Research and Education in Health</a>, a fellow of the <a href="https://www.aasciences.africa/">African Academy of Science</a> and a member of the America Science Honors Society (Sigma Xi).</p>
<p>With 27 years as a professor, he was one of the longest serving professors in the university. He contributed a great deal in this capacity. He held much of our institution’s history and memories. He served at different periods as head of department and dean. He was also on many committees of the university. </p>
<h2>Excellent mentor</h2>
<p>Olaleye’s interest in the career development of young people was outstanding. He had a passion for mentoring. I met him in 1993 when I came to Virology for my master’s programme. That first encounter is well documented in <a href="https://www.ui.edu.ng/gallery/professor-georgina-njideka-odaibo-department-virology-faculty-basic-medical-sciences">my inaugural lecture</a> of 27 June 2019. It instilled in me the spirit and attitude of hard work, commitment and dedication, and the sense of being ever ready. He was the giant who provided the shoulders for me and many others to stand on. </p>
<p>He mentored many who are at the peak of their careers today. We are from diverse specialities, in different parts of the globe. In appreciation of his commitment, dedication and sacrifices made towards our career development, we celebrated him on his 60th birthday in 2014. I’m happy that he heard all the kind things we said about him. </p>
<h2>Brilliant researcher</h2>
<p>He was a great researcher. His research focused on diagnosis, characterisation and molecular epidemiology of various virus-related diseases in Nigeria. He had collaborators from different parts of the world and was principal investigator, co-principal investigator and investigator of many research grants. He attracted one of the highest number of <a href="https://www.com.ui.edu.ng/index.php/prof-olufemi-d-olaleye">grants</a> - in terms of number and dollar value - to the University of Ibadan. He published <a href="https://scholar.google.com/citations?user=prVk8WkAAAAJ&hl=en">over 200 papers</a> in reputable international journals.</p>
<p>One of the major breakthroughs of his research was the <a href="https://www.com.ui.edu.ng/index.php/prof-olufemi-d-olaleye">first</a> isolation and characterisation of the 2nd HIV recombinant form (CRF02) during his Fogarty International Research Fellowship programme at the University of Southern California, Los Angeles, from September 1990 to September 1992. This virus strain, which he named IbNg (for Ibadan, Nigeria), has been shown to be the <a href="https://link.springer.com/referenceworkentry/10.1007%2F978-1-4939-7101-5_34">predominant strain</a> circulating in West Africa and a good candidate for vaccine development in the region. </p>
<h2>Forthright and selfless</h2>
<p>Olaleye was honest, peace-loving and opposed injustice. Not only to him, but to anyone at all, even those he did not know. He was hardworking and he appreciated hard work. He would not trade merit for sentiments or tribalism. </p>
<p>He was a forthright person, outspoken and truthful. He respected everyone, irrespective of age and gender. He was humility personified.</p>
<p>Olaleye was a system person and a patriotic Nigerian who would always consider the system above his personal interest. He was at the <a href="https://www.vanguardngr.com/2021/07/makinde-mourns-top-ui-virologist-professor-olaleye/">forefront</a> of Oyo State’s response to the COVID-19 pandemic and the state governor attested to this in his tribute. </p>
<p>He invested in capacity development, especially research capacity (infrastructural and human). With grants from the National Institute for Health in the USA, he spearheaded training on research capacity development for faculty and postgraduate students in six universities in Nigeria. </p>
<p>During his tenure as Dean of the Faculty of Basic Medical Sciences from 2006 to 2010, he established a faculty conference, UniIbadan Conference of Biomedical Research. One of its objectives was to create a platform for young scientists in the country to show case their work, learn new ideas and establish networks required for career growth.</p>
<p>Some 20 years ago, no one wanted to come to the Department of Virology. But today, the story is different. Now people ask, why are you <em>not</em> in virology? It took the efforts, hard work, dedication and commitment of Olaleye to initiate changes to the department. With funds from his grants and support from funders, the department was renovated and equipped. </p>
<p>He successfully led a team of well-motivated academic and technical staff of the department to obtain World Health Organization Africa Region/ SLIPTA laboratory certification and the SANAS laboratory quality accreditation (ISO 15189) in 2018. </p>
<p>Professor David Olufemi Olaleye served his community selflessly and meritoriously. Sustaining his legacy is our assignment now.</p><img src="https://counter.theconversation.com/content/166199/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Georgina Njideka Odaibo does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Nigeria’s academic community is mourning the death of virology professor and leading researcher, David Olufemi Olaleye.Georgina Njideka Odaibo, Professor of Virology and Specialist Adviser, University College Hospital, Ibadan, University of IbadanLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1632542021-06-24T20:12:34Z2021-06-24T20:12:34ZWe found traces of humanity’s age-old arms race with coronaviruses written in our DNA<figure><img src="https://images.theconversation.com/files/408097/original/file-20210624-27-1nygxjy.jpg?ixlib=rb-1.1.0&rect=27%2C9%2C3027%2C2377&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.flickr.com/photos/niaid/49534865371/">NIAID-RML</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>A coronavirus may have swept across East Asia more than 20,000 years ago, leaving traces in the DNA of people in modern China, Japan and Vietnam. Our research, <a href="https://doi.org/10.1016/j.cub.2021.05.067">published</a> in Current Biology, found evidence of genetic adaptation to the coronavirus family of viruses in 42 genes in modern populations in these regions.</p>
<p>The COVID-19 pandemic, caused by the coronavirus SARS-CoV-2, is so far responsible for more than 3.8 million deaths and billions of dollars in economic losses worldwide. The coronavirus family also includes the related MERS and SARS viruses, both of which have caused significant deadly outbreaks in the past 20 years.</p>
<p>Our results show how the hunt for genetic traces of historical viral outbreaks may help us treat the outbreaks of the future.</p>
<h2>Pandemics may be as old as human history</h2>
<p>We have had pandemics before. In the 20th century alone, three variants of the influenza virus each resulted in wide-ranging outbreaks that killed millions: the “Spanish Flu” of 1918-20, the “Asian Flu” of 1957-58, and the “Hong Kong Flu” of 1968-69. </p>
<p>Historical records of outbreaks caused by viruses and other pathogens stretch back thousands of years. It seems plausible that these interactions go back even further, to the earliest periods of human prehistory. </p>
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Read more:
<a href="https://theconversation.com/this-isnt-the-first-global-pandemic-and-it-wont-be-the-last-heres-what-weve-learned-from-4-others-throughout-history-136231">This isn't the first global pandemic, and it won't be the last. Here's what we've learned from 4 others throughout history</a>
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<p>The ancient migrations that saw our ancestors spread out from Africa across the world would have introduced them to new pathogens. Like many other environmental challenges, these ancient viral encounters may have triggered adaptions that helped our ancestors survive. These adaptations may have included physiological or immunological changes that improved resistance to infection or reduced the health impacts of the disease.</p>
<h2>Adaptation to disease can leave genetic traces</h2>
<p>Over the past few decades, geneticists have devised powerful statistical tools to uncover genetic traces of historical adaptation events that remain present within the genomes of people living today. These tools have allowed scientists to discover genes that mark adaptations for high-altitude living and the adult consumption of milk, among other things.</p>
<p>Our team was curious to see whether historical encounters with ancient coronaviruses have left any such trace in today’s human populations. Besides revealing historical coronavirus outbreaks, this information may hold new insights in the genetic basis of coronavirus infection and how these viruses cause disease in modern humans.</p>
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Read more:
<a href="https://theconversation.com/what-is-a-virus-how-do-they-spread-how-do-they-make-us-sick-133437">What is a virus? How do they spread? How do they make us sick?</a>
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<p>Viruses are simple creatures with one objective: to make more copies of themselves. But their simple biological structure means they cannot reproduce independently. </p>
<p>Instead, they must invade the cells of other organisms and hijack their molecular machinery. Viral invasions involve attaching and interacting with specific proteins produced by the host cell, which we call viral interacting proteins (VIPs).</p>
<h2>The marks of ancient coronavirus</h2>
<p>We applied cutting-edge computational analyses to the genomes of more than 2,500 people from 26 populations around the world. We found signatures of adaptation in 42 different human genes that encode VIPs.</p>
<p>These VIP signals were present in only five populations, all of them from East Asia – the likely ancestral homeland of the coronavirus family. This suggests the ancestors of modern East Asians were initially exposed to coronaviruses around 25,000 years ago.</p>
<p>Further testing revealed that the 42 VIPs are primarily expressed in the lungs, which is the tissue most affected by COVID-19 symptoms. We also confirmed these VIPs interact directly with the SARS-CoV-2 virus responsible for the current pandemic. </p>
<p>Other independent studies have also shown that mutations in VIP genes may mediate SARS-CoV-2 <a href="https://www.nature.com/articles/s41431-020-0636-6">susceptibility</a> and the <a href="https://www.medrxiv.org/content/10.1101/2021.03.10.21252820v2">severity</a> of <a href="https://www.medrxiv.org/content/10.1101/2020.10.06.20205864v1">COVID-19 symptoms</a>. In addition, several VIP genes are either currently being used as drug targets for COVID-19 treatments or are part of clinical trials for this purpose.</p>
<p>Several of the adaptive VIPs identified in our study are also drug targets for other types of viruses, such as Zika virus and hepatitis C. Several of these drugs have been successfully repurposed, and suggests that others could potentially be repurposed for COVID-19 treatment. </p>
<p>By uncovering the genes impacted by historical viral outbreaks, our study points to the promise of evolutionary genetic analyses as a new tool for fighting future outbreaks.</p><img src="https://counter.theconversation.com/content/163254/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>The authors do not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and have disclosed no relevant affiliations beyond their academic appointment.</span></em></p>New DNA evidence shows humans may have been battling coronaviruses for longer than recorded history.Yassine Souilmi, Visiting Investigator, Australian National UniversityRay Tobler, Postdoctoral fellow, Australian National UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1624932021-06-21T12:21:04Z2021-06-21T12:21:04ZWhy gain-of-function research matters<figure><img src="https://images.theconversation.com/files/407279/original/file-20210618-12-jbsi1e.jpg?ixlib=rb-1.1.0&rect=54%2C9%2C5948%2C3956&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">In February 2021, a World Health Organization team investigating the origins of COVID-19 visited the Wuhan Institute of Virology in Wuhan, China.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/peter-daszak-thea-fischer-and-other-members-of-the-world-news-photo/1230937740">Hector Retamal/AFP via Getty Images</a></span></figcaption></figure><p><em>Due to unanswered questions into the origins of the coronavirus pandemic, both the <a href="https://www.whitehouse.gov/briefing-room/statements-releases/2021/05/26/statement-by-president-joe-biden-on-the-investigation-into-the-origins-of-covid-19/">U.S. government</a> and <a href="https://science.sciencemag.org/content/372/6543/694.1">scientists</a> have called for a deeper examination into the validity of claims that a virus could have escaped from a lab in Wuhan, China.</em></p>
<p><em>Much of the discussion surrounds “gain-of-function” research. So The Conversation asked <a href="https://scholar.google.com/citations?user=CcisQ1kAAAAJ&hl=en">David Gillum</a> and <a href="https://scholar.google.com/citations?user=YkYvOhoAAAAJ&hl=en">Rebecca Moritz</a>, who work closely with virologists on a day-to-day basis to ensure the safety and security of the research, and <a href="https://scholar.google.com/citations?user=GwJ0SvMAAAAJ&hl=en">Sam Weiss Evans</a> and <a href="https://scholar.google.com/citations?user=JtIC7noAAAAJ&hl=en">Megan Palmer</a>, who are science and technology policy experts, to explain what this term means and why this kind of research is important.</em></p>
<h2>What does gain of function mean?</h2>
<p>Any organism can acquire a new ability or property, or “gain” a “function.” This can happen through natural selection or a researcher’s experiments. In research, many different types of experiments generate functions, and some pose certain safety and security concerns. </p>
<p>Scientists use a variety of techniques to modify organisms depending on the properties of the organism itself and the end goal. Some of these methods involve directly making changes at the level of genetic code. Others may involve placing organisms in environments that select for functions linked to genetic changes. </p>
<p>Gain of function can occur in an organism in either nature or the laboratory. Some lab examples include creating more <a href="https://www.pnas.org/content/98/20/11444.short">salt- and drought-resistant plants</a> or modifying disease vectors to produce mosquitoes that are <a href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008103">resistant to transmitting dengue fever</a>. Gain of function can also be useful for environmental reasons, such as modifying <em>E. coli</em> so that it can <a href="https://www.washingtonpost.com/food/2021/06/15/plastic-bottles-vanilla-ecoli/">convert plastic waste into a valuable commodity</a>.</p>
<p>In the current debate around SARS-CoV-2, the virus that causes COVID-19, gain of function has a much narrower meaning related to a virus becoming easier to move between humans, or becoming more lethal in humans. It is important to remember, though, that the term “gain of function” by itself covers much more than this type of research.</p>
<h2>Why would researchers do gain-of-function work on potentially dangerous pathogens?</h2>
<p>Gain-of-function experiments may help researchers test scientific theories, develop new technologies and find treatments for infectious diseases. For example, in 2003, when the <a href="https://www.cdc.gov/about/history/sars/timeline.htm">original SARS-CoV outbreak</a> occurred, researchers developed a method to study the virus in the laboratory. One of the experiments was to <a href="https://pubmed.ncbi.nlm.nih.gov/17222058/">grow the virus in mice</a> so they could study it. This work led to a model for researching the virus and testing potential vaccines and treatments.</p>
<p>Gain-of-function research that focuses on potential pandemic pathogens has been supported on the premise that it will help researchers better understand the evolving pathogenic landscape, be better prepared for a pandemic response and develop treatments and countermeasures. </p>
<p>But critics argue that this research to anticipate potential pandemic pathogens does not lead to substantial benefit and is not worth the potential risks. And they say getting out ahead of such threats can be achieved through other means – biological research and otherwise. For instance, the current pandemic has provided numerous lessons on the social and behavioral dynamics of disease prevention measures, which could lead to robust new research programs on the cultural aspects of pandemic preparedness. Understanding when the risks of gain-of-function research outweigh the potential benefits and alternatives, therefore, continues to be subject to debate.</p>
<h2>What are some examples of gain-of-function research, and how risky is it?</h2>
<p>Some potential outcomes of gain-of-function research may include the creation of organisms that are more transmissible or more virulent than the original organism. Other examples include engineering organisms that can evade current detection methods and available treatments, or grow in another part of an organism, such as the ability to cross the blood-brain barrier. </p>
<p>There is no such thing as zero risk in conducting experiments. So the question is whether certain gain-of-function research can be performed at an acceptable level of safety and security by utilizing <a href="https://www.frontiersin.org/articles/10.3389/fbioe.2020.613253/full">risk-mitigation measures</a>. These strategies for reducing risk include the use of biocontainment facilities, exposure control plans, strict operating procedures and training, incident response planning and much more. These efforts involve dedication and meticulous attention to detail at multiple levels of an institution. </p>
<p>Lab incidents will still occur. A robust biosafety and biosecurity system, along with appropriate institutional response, helps to ensure that these incidents are inconsequential. <a href="https://science.sciencemag.org/content/367/6482/1057">The challenge</a> is to make sure that any research conducted – gain-of-function or otherwise – doesn’t pose unreasonable risks to researchers, the public and the environment. </p>
<p>Determining whether specific experiments with potential pathogens should be conducted remains a difficult and contentious topic.</p>
<h2>How do experts determine which gain-of-function research poses too much risk?</h2>
<p>There are multiple ways to answer this question. The first is if the research is intended to develop a biological weapon. The <a href="https://www.un.org/disarmament/biological-weapons/">United Nations Biological Weapons Convention</a>, which went into effect in 1975, forbids state parties from developing, producing, stockpiling, or otherwise acquiring or sharing biological agents, toxins and equipment that have no justification for peaceful or defensive purposes. There should be no research, then, whether gain-of-function or otherwise, that seeks to purposefully develop a biological weapon.</p>
<p>Another way to answer the question is by focusing on the content of the research, rather than its intent. Through experience, researchers and governments have developed lists of both experiments and organisms that need additional oversight because of their potential safety and security risks. One example of this arose when flu researchers placed a self-imposed pause on gain-of-function research involving the transmissibility of highly pathogenic avian influenza H5N1 viruses in 2012. The U.S. government subsequently <a href="https://journals.asm.org/doi/full/10.1128/mBio.00379-12">imposed a moratorium</a> on the work in 2014. Both moratoriums were lifted by the end of 2017 following a lengthy debate and study of the risks and the development of additional oversight and reporting requirements.</p>
<p>In the past decade, the United States has developed oversight for research that could be directly misused for <a href="https://osp.od.nih.gov/biotechnology/dual-use-research-of-concern/">nefarious purposes</a>. This includes policies on
“<a href="https://osp.od.nih.gov/biotechnology/dual-use-research-of-concern/">dual-use research of concern</a>” (DURC) and policies on “<a href="https://osp.od.nih.gov/biotechnology/gain-of-function-research/">pathogens of pandemic potential</a>” enhanced to gain transmissibility or virulence. </p>
<p>[<em>Over 100,000 readers rely on The Conversation’s newsletter to understand the world.</em> <a href="https://theconversation.com/us/newsletters/the-daily-3?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=100Ksignup">Sign up today</a>.]</p>
<p>The main point is that our understanding is constantly evolving. Just before the COVID-19 pandemic began, <a href="https://osp.od.nih.gov/wp-content/uploads/NSABB_January_2020_Meeting_Minutes.pdf">the U.S. government had started to review and update its policies</a>. It is an open question what lessons will be learned from this pandemic, and how that will reshape our understanding of the value of gain-of-function research. One thing that is likely to happen, though, is that we will rethink the assumptions we have been making about the relationships between biological research, security and society. This may be an opportunity to <a href="https://science.sciencemag.org/content/368/6487/138.full">review and enhance</a> systems of biosecurity and biosafety governance.</p><img src="https://counter.theconversation.com/content/162493/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>David Gillum is the past president of the American Biological Safety Association (ABSA) International. He is a past-judge and member of the safety and security committee for the International Genetically Engineered Machine Competition.</span></em></p><p class="fine-print"><em><span>Megan J. Palmer receives funding from the Open Philanthropy Project and the Nuclear Threat Initiative. She is on the Council of the Engineering Biology Research Consortium, co-chairs a World Economic Forum Global Future Council on Synthetic Biology, is an Advisor to the International Genetically Engineered Machine Competition, is a member of a World Health Organization Working Group on the Responsible Use of Life Sciences, and is a member of the Board of Directors of Revive and Restore.</span></em></p><p class="fine-print"><em><span>Sam Weiss Evans receives funding from the Schmidt Futures Foundation. He is a member of the Engineering Biology Research Consortium’s Security Working Group, and an Advisor to the international Genetically Engineered Machines Competition. </span></em></p><p class="fine-print"><em><span>Rebecca Moritz does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The research community is taking a closer look at the lab-leak hypothesis for the origin of COVID-19, prompting discussion about the risks and benefits of engineering viruses.David Gillum, Senior Director of Environmental Health and Safety and Chief Safety Officer, Arizona State UniversityRebecca Moritz, Biosafety Director and Responsible Official, Colorado State UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1618792021-06-14T20:09:37Z2021-06-14T20:09:37ZIs a hybrid COVID strain behind Vietnam’s latest wave? Not exactly<p>We recently heard a new “hybrid variant” of the coronavirus has been detected <a href="https://www.abc.net.au/news/2021-05-29/vietnam-detects-new-coronavirus-variant/100176522">in Vietnam</a>, amid a spike in cases in the country. </p>
<p>The variant was originally described as a hybrid of the UK (now Alpha) and Indian (now Kappa B.1.617.1 and Delta B.1.617.2) strains of the virus. But what does this actually mean? And if we look at the science behind virus behaviour, is a hybrid really what we’re seeing?</p>
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<h2>What is a ‘hybrid’?</h2>
<p>In virology, the scientific name for a hybrid is a “recombinant”. Recombination is when two strains infect a person at the same time and <a href="https://www.nature.com/articles/nrmicro2614">combine</a> to make a new strain.</p>
<p>This process is common in influenza, where it’s often called an “<a href="https://www.euro.who.int/en/health-topics/communicable-diseases/influenza/pandemic-influenza/how-pandemic-influenza-emerges">antigenic shift</a>”.</p>
<p>The major concern with viral recombination is the possibility the new strain will rapidly emerge with advantages of both strains, and you’ll get, for example, a strain that’s both more transmissible and faster at replicating. The same can be true for gradual mutation, but this takes more time.</p>
<p>Emerging evidence suggests coronaviruses can undergo recombination, which may have contributed to <a href="https://www.nature.com/articles/s41598-020-78703-6">the origins of SARS-CoV-2</a>, the virus that causes COVID-19. There’s <a href="https://www.news-medical.net/news/20210310/Analysis-shows-moderate-evidence-for-SARS-CoV-2-recombination.aspx">moderate evidence</a> SARS-CoV-2 itself has undergone some recent recombination, with early reports suggesting <a href="https://www.newscientist.com/article/2268379-two-coronavirus-variants-have-merged-heres-what-you-need-to-know/">a possible recombination</a> event between an Alpha (B.1.1.7) and Epsilon (B.1.429) variant. </p>
<p>It’s important to note these reports are early and some of the science is <a href="https://www.biorxiv.org/content/10.1101/2021.03.07.434287v1">not yet peer-reviewed</a>. So, the role of recombination in the evolution of SARS-CoV-2 still needs to be confirmed. </p>
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Read more:
<a href="https://theconversation.com/whats-the-difference-between-mutations-variants-and-strains-a-guide-to-covid-terminology-154825">What's the difference between mutations, variants and strains? A guide to COVID terminology</a>
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<img alt="A graph depicting recombination versus accumulated mutations." src="https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=922&fit=crop&dpr=1 600w, https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=922&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=922&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1158&fit=crop&dpr=1 754w, https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1158&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/405847/original/file-20210611-27-1fnrmso.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1158&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="attribution"><span class="source">Lara Herrero</span>, <span class="license">Author provided</span></span>
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<p>According to early reports from the World Health Organization (WHO), genetic sequencing is now showing the strain circulating in Vietnam is a Delta strain that has developed <a href="https://asia.nikkei.com/Editor-s-Picks/Interview/Vietnam-s-new-COVID-variant-part-of-existing-Indian-strain-WHO">some additional mutations</a>.</p>
<p>Scientifically, and <a href="https://www.forbes.com/sites/roberthart/2021/06/03/no-new-hybrid-variant-in-vietnam-world-health-organization-official-says/?sh=e1d22dd3aee2">according to the WHO</a>, this means it’s not a “hybrid” at all. Rather, it’s a mutated version of the Delta variant.</p>
<p>The Delta variant was originally detected in India and has since spread around the world, <a href="https://theconversation.com/whats-the-delta-covid-variant-found-in-melbourne-is-it-more-infectious-and-does-it-spread-more-in-kids-a-virologist-explains-162170">including to Australia</a>. Early reports suggest it’s more transmissible and possibly more deadly than other variants, leading health authorities, including in Vietnam, to be on high alert. </p>
<p>We don’t yet know the details of which extra mutations are found in the Vietnam version of the Delta variant. But <a href="https://www.cdc.gov/coronavirus/2019-ncov/science/science-briefs/scientific-brief-emerging-variants.html">we have seen</a> this phenomenon before, where mutations known in one variant are reported as accumulating in a different SARS-CoV-2 variant.</p>
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<img alt="An infographic depicting recombination versus accumulated mutations." src="https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=408&fit=crop&dpr=1 600w, https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=408&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=408&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=513&fit=crop&dpr=1 754w, https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=513&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/405860/original/file-20210611-21-19fgbi2.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=513&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Recombination is when two strains of a virus infect a person at the same time and combine to form a new strain.</span>
<span class="attribution"><span class="source">Lara Herrero, created using BioRender</span>, <span class="license">Author provided</span></span>
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<h2>What we know, and don’t know</h2>
<p>Late last month, Vietnamese health officials reported this so-called hybrid variant circulating was very dangerous and <a href="https://www.abc.net.au/news/2021-05-29/vietnam-detects-new-coronavirus-variant/100176522">more transmissible</a> than other strains of the virus. They said it was behind the <a href="https://covid19.who.int/region/wpro/country/vn">surge in infections</a> Vietnam experienced during May. </p>
<p>These initial reports were based on clinical observations. Whether this mutated variant is more infectious, and the degree to which it can be implicated in Vietnam’s current surge of infections, is not yet certain.</p>
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Read more:
<a href="https://theconversation.com/whats-the-delta-covid-variant-found-in-melbourne-is-it-more-infectious-and-does-it-spread-more-in-kids-a-virologist-explains-162170">What's the Delta COVID variant found in Melbourne? Is it more infectious and does it spread more in kids? A virologist explains</a>
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<p>When someone is diagnosed with COVID-19, it’s not always common to perform <a href="https://www.phgfoundation.org/blog/wgs-to-combat-COVID-19">whole-genome sequencing</a> on their viral sample. It’s often an expensive and time-consuming process undertaken by public health officials, epidemiologists and virologists <a href="https://www.nature.com/articles/s41467-020-18314-x">to understand and predict</a> the movement of an outbreak. </p>
<p>This means not all countries will have the capacity to rapidly provide whole-genome SARS-CoV-2 sequences. So the exact details of what strain is circulating where will always come after reports of case numbers.</p>
<p>It’s likely we don’t yet know if this altered Delta strain is the predominant one circulating in Vietnam. Vietnam has either not yet conducted full analysis of genomic data from enough patient samples, or is yet to make this information publicly available. </p>
<p>Additionally, we don’t yet know whether this mutated variant is more transmissible or causes more severe COVID-19 than the Delta variant or the original SARS-CoV-2. We also don’t know whether it will affect how well COVID vaccines work. </p>
<p>To answer these questions, we’ll need more detailed genomic data, time to see how things play out in the community, as well as data from scientific and clinical studies involving people infected with this variant. </p>
<h2>New names</h2>
<p>As the COVID-19 pandemic continues to evolve, so too do the SARS-CoV-2 strains driving the chaos.</p>
<p>Initially reports focused on the “<a href="https://theconversation.com/the-uk-variant-is-likely-deadlier-more-infectious-and-becoming-dominant-but-the-vaccines-still-work-well-against-it-156951">UK variant</a>” or the “<a href="https://theconversation.com/whats-the-indian-variant-responsible-for-victorias-outbreak-and-how-effective-are-vaccines-against-it-161574">Indian variant</a>”, and so on.</p>
<p>Recognising the need for a universal naming system, the <a href="https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/">WHO has assessed</a> the genomic classification of strains and provided new, more general names based on the Greek alphabet.</p>
<p>This list includes both “variants of interest” and “variants of concern”. While Delta is classified as a variant of concern, this altered Delta variant detected in Vietnam is not listed at this stage.</p>
<p>To be considered as a new variant of the virus, or strain, a variant needs to <a href="https://theconversation.com/whats-the-difference-between-mutations-variants-and-strains-a-guide-to-covid-terminology-154825">show distinct physical properties</a>, and therefore behave differently, from the original virus or an existing strain. From the WHO’s perspective, this doesn’t appear to be the case for the mutated Delta strain. At least not yet.</p>
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Read more:
<a href="https://theconversation.com/coronavirus-variants-have-new-names-we-can-finally-stop-stigmatising-countries-159652">Coronavirus variants have new names: we can finally stop stigmatising countries</a>
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<h2>A stark reminder</h2>
<p>Vietnam was a country that prided itself on containing the virus, with initial success in border control and public health measures. This resulted in <a href="https://www.bbc.com/news/world-asia-52628283">periods without community transmission</a>. At the moment, it’s recording more than 200 new cases a day (on <a href="https://covid19.who.int/region/wpro/country/vn">June 10</a> there were 413). </p>
<p>Hybrid strain or not, Vietnam’s situation should be a reminder to the world — and particularly countries like Australia, with a similarly good track record in containing the virus — of the continued importance of social distancing and vaccination in our fight against COVID-19.</p><img src="https://counter.theconversation.com/content/161879/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lara Herrero does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>We recently heard reports of a new and dangerous ‘hybrid’ variant circulating in Vietnam. There is such as a thing as a hybrid viral variant — but this doesn’t appear to be it.Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1613872021-06-07T12:34:25Z2021-06-07T12:34:25ZHow virus detectives trace the origins of an outbreak – and why it’s so tricky<figure><img src="https://images.theconversation.com/files/403850/original/file-20210601-23-kb2qfx.jpg?ixlib=rb-1.1.0&rect=0%2C12%2C8192%2C4549&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The prevention of future pandemics requires examining viral family trees.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/corona-virus-under-magnifying-glass-observation-royalty-free-image/1204860249?adppopup=true">Stockcrafter/iStock via Getty Images Plus</a></span></figcaption></figure><p>Every time there is a major disease outbreak, one of the first questions scientists and the public ask is: “Where did this come from?”</p>
<p>In order to predict and prevent future pandemics like COVID-19, researchers need to find the origin of the viruses that cause them. This is not a trivial task. The <a href="https://doi.org/10.1038/428820a">origin of HIV</a> was not clear until 20 years after it spread around the world. Scientists still don’t know the origin of Ebola, even though it has <a href="https://doi.org/10.15252/emmm.201404792">caused periodic epidemics since the 1970s</a>.</p>
<p>As an <a href="https://plantpath.psu.edu/directory/mjr25">expert in viral ecology</a>, I am often asked how scientists trace the origins of a virus. In my work, I have found many new viruses and some well-known pathogens that infect wild plants <a href="https://doi.org/10.1146/annurev-genet-110711-155600">without causing any disease</a>. Plant, animal or human, the methods are largely the same. Tracking down the origins of a virus involves a combination of extensive fieldwork, thorough lab testing and quite a bit of luck.</p>
<h2>Viruses jump from wild animal hosts to humans</h2>
<p>Many viruses and other disease agents that infect people originate in animals. These diseases are <a href="https://doi.org/10.4103/1995-7645.277535">zoonotic</a>, meaning they are caused by animal viruses that jumped to people and adapted to spread through the human population.</p>
<p>It might be tempting to start the viral origin search by testing sick animals at the site of the first known human infection, but wild hosts often don’t show any symptoms. Viruses and their hosts adapt to each other over time, so viruses often don’t cause obvious disease symptoms until they’ve <a href="https://doi.org/10.15252/embr.202051374">jumped to a new host species</a>. Researchers can’t just look for sick animals.</p>
<p>Another problem is that people and their food animals aren’t stationary. The place where researchers find the first infected person is not necessarily close to the place where the virus first emerged.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Researcher in PPE holding pipette in lab." src="https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/403854/original/file-20210601-23-1shk7oe.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">A challenge in viral origin tracing is the wide range of human and animal samples that need to be collected and tested.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/researcher-working-in-a-biochemist-laboratory-royalty-free-image/1301584009?adppopup=true">LLuis Alvarez/DigitalVision via Getty Images</a></span>
</figcaption>
</figure>
<p>In the case of COVID-19, bats were an obvious first place to look. They’re known hosts for many coronaviruses and are the probable source of other zoonotic diseases like SARS and <a href="https://www.cdc.gov/coronavirus/mers/index.html">MERS</a>.</p>
<p>For SARS-CoV-2, the virus that causes COVID-19, the nearest relative scientists have found so far is <a href="https://doi.org/10.1038/s41586-020-2012-70">BatCoV RaTG13</a>. This virus is part of a collection of bat coronaviruses discovered in 2011 and 2012 by virologists from the Wuhan Virology Institute. The virologists were looking for SARS-related coronaviruses in bats after the <a href="https://theconversation.com/the-mysterious-disappearance-of-the-first-sars-virus-and-why-we-need-a-vaccine-for-the-current-one-but-didnt-for-the-other-137583">SARS-CoV-1 pandemic in 2003</a>. They collected fecal samples and throat swabs from bats at a site in Yunnan Province about 932 miles (1,500 kilometers) from the institute’s lab in Wuhan, where they brought samples back for further study.</p>
<p>To test whether the bat coronaviruses could spread into people, researchers infected monkey kidney cells and <a href="https://osp.od.nih.gov/scientific-sharing/hela-cells-landing/">human tumor-derived cells</a> with the Yunnan samples. They found that a number of the viruses from this collection could <a href="https://doi.org/doi:10.1128/JVI.02582-15.">replicate in the human cells</a>, meaning they could potentially be transmitted directly from bats to humans without an intermediate host. Bats and people don’t come into direct contact very often, however, so an intermediate host is still quite likely.</p>
<h2>Finding the nearest relatives</h2>
<p>The next step is to determine how closely related a suspected wildlife virus is to the one infecting humans. Scientists do this by figuring out the genetic sequence of the virus, which involves determining the order of the basic building blocks, or <a href="https://www.nature.com/scitable/topicpage/the-order-of-nucleotides-in-a-gene-6525806/">nucleotides</a>, that make up the genome. The more nucleotides two genetic sequences share, the more closely related they are.</p>
<p>Genetic sequencing of bat coronavirus RaTG13 showed it to be over <a href="https://www.nature.com/articles/s41586-020-2012-7">96% identical</a> to SARS-CoV-2. This level of similarity means that RaTG13 is a pretty close relative to SARS-CoV-2, confirming that SARS-CoV-2 probably originated in bats, but is still too distant to be a direct ancestor. There likely was another host that caught the virus from bats and passed it on to humans.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Person wearing respirator, gloves, and headlamp holding bat up to the light." src="https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=406&fit=crop&dpr=1 600w, https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=406&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=406&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=510&fit=crop&dpr=1 754w, https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=510&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/404078/original/file-20210602-13-1wk0cse.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=510&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">In order to find the intermediate host between bats and humans, researchers have to cast a large net and sample many different animals.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/APTOPIXBrazilRacingforaRemedy-NextPandemic/28c42902d3c8492096c99f2ad694a984/photo?boardId=58e13cbbaf024f5dbdb2431332c5a934&st=boards&mediaType=audio,photo,video,graphic&sortBy=&dateRange=Anytime&totalCount=5&currentItemNo=2">AP Photo/Silvia Izquierdo</a></span>
</figcaption>
</figure>
<p>Because some of the earliest cases of COVID-19 were found in people associated with the wildlife market in Wuhan, there was speculation that a wild animal from this market was the intermediate host between bats and humans. However, researchers <a href="https://www.livescience.com/covid-19-did-not-start-at-wuhan-wet-market.html">never found the coronavirus</a> in animals from the market. </p>
<p>Likewise, when a related coronavirus was identified in <a href="https://doi.org/0.1038/s41586-020-2169-0">pangolins</a> confiscated in an anti-smuggling operation in southern China, many leaped to the conclusion that SARS-CoV-2 had jumped from bats to pangolins to humans. The <a href="https://doi.org/10.1371/journal.ppat.1008421">pangolin virus</a> was found to be only 91% identical to SARS-CoV-2, though, making it unlikely to be a direct ancestor of the human virus.</p>
<p>To pinpoint the origin of SARS-CoV-2, a lot more wild samples need to be collected. This is a difficult task – sampling bats is time-consuming and requires strict precautions against accidental infection. Since SARS-related coronaviruses are found in <a href="https://doi.org/10.1038/s41467-021-21240-1">bats across Asia</a>, including Thailand and Japan, it’s a very big haystack to search for a very small needle.</p>
<h2>Creating a family tree for SARS-CoV-2</h2>
<p>In order to sort out the puzzle of viral origins and movement, scientists not only have to find the missing pieces, but also figure out how they all fit together. This requires collecting viral samples from human infections and comparing those genetic sequences both to each other and to other animal-derived viruses.</p>
<p>To determine how these viral samples are related to each other, researchers use computer tools to construct the virus’s family tree, or <a href="https://dx.doi.org/10.1016%2FB978-0-12-801238-3.95723-4">phylogeny</a>. Researchers compare the genetic sequences of each viral sample and construct relationships by aligning and ranking genetic similarities and differences.</p>
<p>The direct ancestor to the virus, sharing the greatest genetic similarity, could be thought of as its parent. Variants sharing that same parent sequence but with enough changes to make them distinct from each other are like siblings. In the case of SARS-CoV-2, the <a href="https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/">South African variant, B.1.351, and the U.K. variant, B.1.1.7</a>, are siblings.</p>
<p>Building a family tree is complicated by the fact that different analysis parameters can give different results: The same set of genetic sequences can produce two very different family trees.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Example of two different phylogenetic trees constructed for the same genetic sequences" src="https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=451&fit=crop&dpr=1 600w, https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=451&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=451&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=567&fit=crop&dpr=1 754w, https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=567&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/404132/original/file-20210602-15-5xrxh.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=567&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">The nucleotide sequences of six fictional viruses are shown on the top. Below are two family trees of these viruses created using two different programs. The tree on the left uses only percent identity, while the tree on the right also considers whether the two sequences share similar characters.</span>
<span class="attribution"><span class="source">Marilyn Roossinck</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>For SARS-CoV-2, phylogenetic analysis proves particularly difficult. Though <a href="https://nextstrain.org/ncov/global">tens of thousands of SARS-CoV-2 sequences</a> are now available, they don’t differ from one another enough to <a href="https://doi.org/10.1093/molbev/msaa314">form a clear picture</a> of how they’re related to each other. </p>
<h2>The current debate: Wild host or lab spillover?</h2>
<p>Could SARS-CoV-2 have been released from a research lab? Although <a href="https://www.who.int/publications/i/item/who-convened-global-study-of-origins-of-sars-cov-2-china-part">current evidence</a> implies that this is not the case, 18 prominent virologists recently suggested that this question should be <a href="https://science.sciencemag.org/content/372/6543/694.1">further investigated</a>.</p>
<p>Although there has been speculation about SARS-CoV-2 being engineered in a lab, this possibility seems highly unlikely. When comparing the genetic sequence of wild RaTG13 with SARS-CoV-2, differences are randomly spread across the genome. In an engineered virus, there would be clear blocks of changes that represent <a href="https://doi.org/10.1016/j.meegid.2021.104812">introduced sequences</a> from a different viral source.</p>
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<p>There is one unique sequence in the SARS-CoV-2 genome that codes for a part of the spike protein that seems to play an important role in infecting people. Interestingly, a similar sequence is found in the MERS coronavirus that <a href="https://doi.org/10.21873/invivo.12384">causes a disease similar to COVID-19</a>.</p>
<p>Though it is not clear how SARS-CoV-2 acquired these sequences, viral evolution suggests they arose from natural processes. Viruses <a href="https://doi.org/10.1002/9780470015902.a0000436.pub3">accumulate changes</a> either by genetic exchange with other viruses and their hosts, or by random mistakes during replication. Viruses that gain a genetic change that gives them a <a href="https://doi.org/10.1002/9780470015902.a0000436.pub3">reproductive advantage</a> would typically continue to pass it on through replication. That MERS and SARS-CoV-2 share a similar sequence in this part of the genome suggests that it naturally evolved in both and spread because it helps them infect human cells.</p>
<h2>Where to go from here?</h2>
<p>Figuring out the origin of SARS-CoV-2 could give us clues to understand and predict future pandemics, but we may never know exactly where it came from. Regardless of how the SARS-CoV-2 jumped into humans, it’s here now, and it’s probably here to stay. Going forward, researchers need to continue monitoring its spread, and get as many people vaccinated as possible.</p><img src="https://counter.theconversation.com/content/161387/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Marilyn J. Roossinck does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Bat hosts, lab leaks – tracing SARS-CoV-2 to its origins involves more than just tracking down patient zero.Marilyn J. Roossinck, Professor of Plant Pathology and Environmental Microbiology, Penn StateLicensed as Creative Commons – attribution, no derivatives.