tag:theconversation.com,2011:/us/topics/viruses-7008/articlesViruses – The Conversation2024-03-11T17:18:48Ztag:theconversation.com,2011:article/2223062024-03-11T17:18:48Z2024-03-11T17:18:48ZThe next pandemic? It’s already here for Earth’s wildlife<p>I am a conservation biologist who studies emerging infectious diseases. When people ask me what I think the next pandemic will be I often say that we are in the midst of one – it’s just afflicting a great many species more than ours.</p>
<p>I am referring to the highly pathogenic strain of avian influenza H5N1 (HPAI H5N1), otherwise known as bird flu, which has killed millions of birds and unknown numbers of mammals, particularly during the past three years. </p>
<p>This is the strain that emerged in domestic geese in China in 1997 and quickly jumped to humans in south-east Asia with a mortality rate of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1634780/">around 40-50%</a>. My research group <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1634780/">encountered the virus</a> when it killed a mammal, an endangered <a href="https://svw.vn/owstons-civet/">Owston’s palm civet</a>, in a captive breeding programme in Cuc Phuong National Park Vietnam in 2005.</p>
<p>How these animals caught bird flu was never confirmed. Their diet is mainly earthworms, so they had not been infected by eating diseased poultry like many captive tigers in the region.</p>
<p>This discovery prompted us to collate all confirmed reports of fatal infection with bird flu to assess just how broad a threat to wildlife this virus might pose.</p>
<p>This is how a newly discovered virus in Chinese poultry came to threaten so much of the world’s biodiversity.</p>
<figure class="align-center ">
<img alt="A person in white overalls operates a forklift carrying dead turkeys." src="https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=399&fit=crop&dpr=1 600w, https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=399&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=399&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=501&fit=crop&dpr=1 754w, https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=501&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/580987/original/file-20240311-22-gzginr.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=501&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">H5N1 originated on a Chinese poultry farm in 1997.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/western-negev-israel-march-18-2006-111241157">ChameleonsEye/Shutterstock</a></span>
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</figure>
<h2>The first signs</h2>
<p>Until December 2005, most confirmed infections had been found in a few zoos and rescue centres in Thailand and Cambodia. Our analysis in 2006 showed that nearly half (48%) of all the different groups of birds (known to taxonomists as “orders”) contained a species in which a fatal infection of bird flu had been reported. These 13 orders comprised 84% of all bird species. </p>
<p>We reasoned 20 years ago that the strains of H5N1 circulating were probably highly pathogenic to all bird orders. We also showed that the list of confirmed infected species included those that were globally threatened and that important habitats, such as Vietnam’s Mekong delta, lay close to reported poultry outbreaks.</p>
<p>Mammals known to be susceptible to bird flu during the early 2000s included primates, rodents, pigs and rabbits. Large carnivores such as Bengal tigers and clouded leopards were reported to have been killed, as well as domestic cats.</p>
<p>Our 2006 paper showed the ease with which this virus crossed species barriers and suggested it might one day produce a pandemic-scale threat to global biodiversity.</p>
<p>Unfortunately, our warnings were correct.</p>
<h2>A roving sickness</h2>
<p>Two decades on, bird flu is killing species from <a href="https://www.theguardian.com/environment/2024/jan/02/polar-bear-dies-from-bird-flu-age-of-extinction">the high Arctic</a> to <a href="https://www.cidrap.umn.edu/avian-influenza-bird-flu/avian-flu-reaches-antarcticas-mainland">mainland Antarctica</a>.</p>
<p>In the past couple of years, bird flu has spread rapidly across Europe and infiltrated North and South America, killing millions of poultry and a variety of bird and mammal species. <a href="https://wwwnc.cdc.gov/eid/article/30/3/23-1098_article">A recent paper</a> found that 26 countries have reported at least 48 mammal species that have died from the virus since 2020, when the latest increase in reported infections started.</p>
<p>Not even the ocean is safe. Since 2020, 13 species of aquatic mammal have succumbed, including American sea lions, porpoises and dolphins, often dying in their thousands in South America. A wide range of scavenging and predatory mammals that live on land are now also confirmed to be susceptible, including mountain lions, lynx, brown, black and polar bears.</p>
<p>The UK alone has <a href="https://www.rspb.org.uk/birds-and-wildlife/seabird-surveys-project-report">lost over 75%</a> of its great skuas and seen a 25% decline in northern gannets. Recent declines in sandwich terns (35%) and common terns (42%) were also <a href="https://maryannsteggles.com/wp-content/uploads/2024/02/Bird-flu-causing-%E2%80%98catastrophic-fall-in-UK-seabird-numbers-conservationists-warn-Bird-flu-The-G.pdf">largely driven by the virus</a>. </p>
<p>Scientists haven’t managed to <a href="https://wwwnc.cdc.gov/eid/article/30/3/23-1098_article">completely sequence</a> the virus in all affected species. Research and continuous surveillance could tell us how adaptable it ultimately becomes, and whether it can jump to even more species. We know it can already infect humans – one or more genetic mutations may make it more infectious.</p>
<h2>At the crossroads</h2>
<p>Between January 1 2003 and December 21 2023, 882 cases of human infection with the H5N1 virus were reported from 23 countries, of which <a href="https://cdn.who.int/media/docs/default-source/influenza/human-animal-interface-risk-assessments/influenza-at-the-human-animal-interface-summary-and-assessment--from-4-october-to-1-november-2023.pdf?sfvrsn=6c67e7df_2&download=true">461 (52%) were fatal</a>.</p>
<p>Of these fatal cases, more than half were in Vietnam, China, Cambodia and Laos. Poultry-to-human infections were first recorded in Cambodia in December 2003. Intermittent cases were reported until 2014, followed by a gap until 2023, yielding 41 deaths from 64 cases. The subtype of H5N1 virus responsible has been detected in poultry in Cambodia since 2014. In the early 2000s, the H5N1 virus circulating had a high human mortality rate, so it is worrying that we are now starting to see people dying after contact with poultry again.</p>
<p>It’s not just H5 subtypes of bird flu that concern humans. The H10N1 virus was originally isolated from wild birds in South Korea, but has also been reported in samples from China and Mongolia. </p>
<p><a href="https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2023.1256090/full">Recent research</a> found that these particular virus subtypes may be able to jump to humans after they were found to be pathogenic in laboratory mice and ferrets. The first person who was confirmed to be infected with H10N5 <a href="https://www.who.int/emergencies/disease-outbreak-news/item/2024-DON504">died</a> in China on January 27 2024, but this patient was also suffering from seasonal flu (H3N2). They had been exposed to live poultry which also tested positive for H10N5.</p>
<p>Species already threatened with extinction are among those which have died due to bird flu in the past three years. The first deaths from the virus in mainland Antarctica have just been <a href="https://www.cidrap.umn.edu/avian-influenza-bird-flu/avian-flu-reaches-antarcticas-mainland">confirmed in skuas</a>, highlighting a looming threat to penguin colonies whose eggs and chicks skuas prey on. Humboldt penguins have already been <a href="https://www.nytimes.com/2023/08/30/science/birds-flu-antarctica.html">killed by the virus</a> in Chile.</p>
<figure class="align-center ">
<img alt="A colony of king penguins." src="https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=399&fit=crop&dpr=1 600w, https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=399&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=399&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=502&fit=crop&dpr=1 754w, https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=502&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/580982/original/file-20240311-26-mmf7j5.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=502&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Remote penguin colonies are already threatened by climate change.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/king-penguin-colony-103683413">AndreAnita/Shutterstock</a></span>
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</figure>
<p>How can we stem this tsunami of H5N1 and other avian influenzas? Completely overhaul poultry production on a global scale. Make farms self-sufficient in rearing eggs and chicks instead of exporting them internationally. The trend towards megafarms containing over a million birds must be stopped in its tracks. </p>
<p>To prevent the worst outcomes for this virus, we must revisit its primary source: the incubator of intensive poultry farms.</p>
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<img alt="Imagine weekly climate newsletter" src="https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/434988/original/file-20211201-21-13avx6y.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<p class="fine-print"><em><span>Diana Bell 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>Bird flu is decimating species already threatened by climate change and habitat loss.Diana Bell, Professor of Conservation Biology, University of East AngliaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2159892024-03-05T03:00:57Z2024-03-05T03:00:57ZLumpy skin disease is a threat to Australia and could decimate our cattle industries – we need to know how it could enter and spread<figure><img src="https://images.theconversation.com/files/577190/original/file-20240221-22-67ggd8.jpg?ixlib=rb-1.1.0&rect=26%2C8%2C5964%2C3979&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/calf-has-sick-lumpy-skin-disease-2028066140">assiduousness, Shutterstock</a></span></figcaption></figure><p>Australian authorities are on high alert amid the spread of <a href="https://www.abc.net.au/news/rural/2022-03-04/lumpy-skin-disease-detected-in-indonesia/100881842">lumpy skin disease</a> in cattle and buffalo across South-East Asia. While <a href="https://www.agriculture.gov.au/biosecurity-trade/pests-diseases-weeds/animal/lumpy-skin-disease/australias-freedom-from-lsd">Australia remains free of the disease</a>, the virus is likely to breach our borders at some stage.</p>
<p>Detection of the disease in Australia’s livestock industries would lead to <a href="https://animalhealthaustralia.com.au/download/1653/">restrictions on cattle, meat and dairy exports</a>, with serious consequences for the economy. </p>
<p>The federal government has a <a href="https://www.agriculture.gov.au/biosecurity-trade/pests-diseases-weeds/animal/lumpy-skin-disease/australias-freedom-from-lsd">plan to detect and respond</a> to an outbreak. But we need to go one better – to predict where the disease is likely to appear and how it might spread. </p>
<p>Our team is developing a model we hope will provide this vital information. It will help Australia prepare and respond not just to the current threat, but to any future biosecurity breach.</p>
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<iframe width="440" height="260" src="https://www.youtube.com/embed/4w58jXPreXg?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Lumpy skin disease is on Australia’s doorstep, with fears the threat is going unnoticed | ABC News (September 2022)</span></figcaption>
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Read more:
<a href="https://theconversation.com/stop-killing-brown-snakes-they-could-be-a-farmers-best-friend-222142">Stop killing brown snakes – they could be a farmer's best friend</a>
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<h2>What is lumpy skin disease?</h2>
<p><a href="https://animalhealthaustralia.com.au/lumpy-skin-disease/">Lumpy skin disease is a viral disease</a> that affects cattle and buffalo, not humans. The incubation period is up to 28 days. </p>
<p>First reported in Zambia in 1929, the <a href="http://www.doi.org/10.14202/vetworld.2022.2764-2771">disease has spread</a> across Africa, the Middle East, Eastern Europe and Asia. It reached <a href="https://www.abc.net.au/news/rural/2022-03-04/lumpy-skin-disease-detected-in-indonesia/100881842">Indonesia in 2022</a>.</p>
<p>Early symptoms include fever and increased tear production. Lumps then appear on the skin and can cover the entire body, gradually hardening as the disease develops. Sometimes the lumps slough off, leaving holes on the skin that are susceptible to infections. </p>
<p>Typically only 1-5% of cattle die from the disease, but those that recover may not return to full health.</p>
<p>Milk production is reduced in cows. Meat yield from infected cattle is likely to be reduced, although it does not contain lumps and is safe to eat. Temporary or permanent infertility in both cows and bulls can also develop during the first month of infection.</p>
<p>The virus is mainly spread by biting insects such as <a href="https://doi.org/10.1136/vr.g5808">mosquitoes, stable flies and ticks</a>. <a href="https://doi.org/10.1007/s11250-021-02786-0">Higher temperature</a> and <a href="https://doi.org/10.1002/vms3.434">increased rainfall</a> can increase insect populations and activity, and have triggered outbreaks of disease overseas.</p>
<p>The disease can also be transmitted by <a href="https://doi.org/10.1186/1297-9716-43-1">close contact between cattle</a>, such as exposure to body fluids.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Map showing where lumpy skin disease has been reported in South-East Asia over the last five years" src="https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=593&fit=crop&dpr=1 600w, https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=593&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=593&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=746&fit=crop&dpr=1 754w, https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=746&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/576654/original/file-20240220-18-l9zg5j.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=746&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Where lumpy skin disease has been reported over the last five years in South-East Asia, as at February 19 this year, using data from the Food and Agriculture Organization of the United Nations.</span>
<span class="attribution"><span class="source">The University of Queensland</span></span>
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<h2>A testing time with Indonesia and Malaysia</h2>
<p>In July last year, Indonesian authorities claimed 13 cows from Australia had <a href="https://www.abc.net.au/news/2023-07-31/lumpy-skin-disease-cattle-from-australia-exports-indonesia/102668870">tested positive</a> days after arrival. At the time, Australian authorities <a href="https://www.agriculture.gov.au/about/news/lsd-detection-in-cattle-exported-to-indonesia">demonstrated</a> that the nation was free of the disease. </p>
<p>Nonetheless, trade between Indonesia and four of Australia’s cattle export holding yards was <a href="https://www.abc.net.au/news/2023-07-30/lsd-in-australian-cattle-in-indonesia/102666812">suspended</a> immediately. Then <a href="https://www.theaustralian.com.au/nation/second-country-suspends-live-cattle-exports-from-australia-over-disease-fears/news-story/d94648994297f0be4497ca0eeda965b5">Malaysia went further and stopped accepting</a> any Australian live cattle and buffalo. </p>
<p><a href="https://www.agriculture.gov.au/about/news/malaysian-authorities-lift-temporary-suspension">Malaysia</a> and <a href="https://www.agriculture.gov.au/about/news/indonesia-lifts-trade-restrictions">Indonesia</a> each lifted their restrictions in early September, after <a href="https://www.agriculture.gov.au/about/news/australia-remains-free-from-lumpy-skin-disease">more than 1,000 cattle</a> were tested across Western Australia, Queensland and the Northern Territory. The Australian government also <a href="https://www.theaustralian.com.au/nation/indonesia-lifts-ban-on-live-cattle-exports-from-australia/news-story/891378279957dfb5dec102a9fe504749">agreed</a> to boost surveillance and biosecurity measures, including testing on farms and <a href="https://www.beefcentral.com/live-export/alec-welcomes-resumption-of-indonesian-cattle-trade/">disinfecting departing export vessels</a>.</p>
<p>Since the lifting of restrictions, the Indonesian government has <a href="https://www.abc.net.au/news/2023-10-11/cattle-rejected-live-export-indonesia-skin-blemishes-lsd/102956626">reportedly</a> rejected Australian cattle with skin blemishes – in some cases, this comprised up to 30% of cattle in a shipment.</p>
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<h2>How could lumpy skin disease enter Australia?</h2>
<p>The Australian government has introduced <a href="https://animalhealthaustralia.com.au/download/1653/">strict biosecurity measures</a> at international ports to minimise the risk of infected animals entering the country. These include disinfection and disinsection (spraying to remove insects) of vessels and cargo.</p>
<p>However, there’s a high risk of <a href="https://www.agriculture.gov.au/sites/default/files/documents/ausvet-lsd-quantitative-assessment.pdf">infected insects entering Australia</a> through international ports or by travelling across the sea to northern Australia. Some infected flying insects may be able to <a href="https://doi.org/10.1111/tbed.12378">cover long distances, aided by strong winds</a>.</p>
<p>Another possible mode of entry for infected insects is through <a href="https://www.abc.net.au/news/rural/2023-12-13/illegal-fishing-in-wa-sparks-biosecurity-fears/103195314">illegal fishers landing on the Australian coast</a>.</p>
<h2>What can be done to prevent the spread of lumpy skin disease?</h2>
<p>In countries where lumpy skin disease is common, <a href="https://doi.org/10.1136/vr.g5808">live vaccines have been used to control the disease</a>. However, this is not practical in disease-free countries such as Australia, because vaccinated animals <a href="https://doi.org/10.1136/vr.i2800">cannot be distinguished</a> from infected animals. This means Australia could not be confirmed free of disease, leading to <a href="https://doi.org/10.1136/vr.g5808">international trade restrictions</a>.</p>
<p>The Australian government <a href="https://minister.agriculture.gov.au/Watt/media-releases/lsd-vaccine-supply-secured">secured a supply of lumpy skin disease vaccines</a> in October. These are being securely stored overseas in case of an outbreak. The vaccines will also be available to neighbouring Papua New Guinea and Timor-Leste.</p>
<p><a href="https://www.woah.org/en/document/lumpy-skin-disease-technical-disease-card/">Preventing the spread of lumpy skin disease</a> requires early detection of the disease, isolation of potentially infected animals and restrictions around their movement. Once initial diagnosis is confirmed, culling of infected animals and insect control would likely follow.</p>
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<h2>What can be done to prepare Australia?</h2>
<p>Australia has a <a href="https://animalhealthaustralia.com.au/download/1653/">veterinary emergency response plan</a> to enact if the disease enters the country. The federal government has also <a href="https://www.agriculture.gov.au/biosecurity-trade/pests-diseases-weeds/animal/lumpy-skin-disease/australias-freedom-from-lsd">boosted surveillance</a> and begun <a href="https://www.agriculture.gov.au/about/news/getting-ready-to-respond">offering training</a> for veterinarians, industry and government staff on how to prevent and control the spread of the disease.</p>
<p>However, innovative models are needed to assess the likely introduction and spread of the disease in Australia. Our team is developing a framework to carry out such modelling. Our model will include data describing the current status of reports of the disease outside of Australia, Australia’s landscape and climate, distribution and movement of cattle, and local insect populations.</p>
<p>These models will produce maps that can be used to identify areas in Australia more suitable to receiving the disease, such as areas with favourable environmental conditions for the survival of imported infected insects. These maps will inform decisions around surveillance and response plans, and help farmers prepare for a potential outbreak of the disease.</p>
<p>Maintaining a high level of preparedness and awareness of the disease among cattle producers, farmers, veterinarians and other relevant individuals is paramount if we are to maintain our disease-free status as an international exporter. </p>
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Read more:
<a href="https://theconversation.com/australias-shot-hole-borer-beetle-invasion-has-begun-but-we-dont-need-to-chop-down-every-tree-under-attack-222610">Australia's shot-hole borer beetle invasion has begun, but we don't need to chop down every tree under attack</a>
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<img src="https://counter.theconversation.com/content/215989/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Kei Owada works for the University of Queensland. The research team at the University of Queensland working on lumpy skin disease modelling is jointly supported by the Queensland Government Department of Agriculture and Fisheries and the University of Queensland.</span></em></p><p class="fine-print"><em><span>Ben Hayes receives funding from the University of Queensland and the Queensland Government Department of Agriculture and Fisheries.</span></em></p><p class="fine-print"><em><span>Ricardo J. Soares Magalhaes receives funding from the University of Queensland and the Queensland Government Department of Agriculture and Fisheries.. </span></em></p><p class="fine-print"><em><span>Timothy J. Mahony works for the University of Queensland. The research team at the University of Queensland working on lumpy skin disease modelling and vaccine development is jointly supported by the Queensland Government Department of Agriculture and Fisheries and the University of Queensland.</span></em></p>A disfiguring disease of cattle and buffalo has arrived on our doorstep. We need to keep lumpy skin disease out of Australia, while preparing for the almost inevitable outbreak.Kei Owada, Postdoctoral Research Fellow, School of Veterinary Science, The University of QueenslandBen Hayes, Director, Centre for Animal Science, The University of QueenslandRicardo J. Soares Magalhaes, Professor, School of Veterinary Science, The University of QueenslandTimothy J. Mahony, Professor, Centre for Animal Science, The University of QueenslandLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2234702024-02-21T13:17:46Z2024-02-21T13:17:46ZWhat is Alaskapox? A microbiologist explains the recently discovered virus that just claimed its first fatality<figure><img src="https://images.theconversation.com/files/575275/original/file-20240211-16-m5e8r4.jpg?ixlib=rb-1.1.0&rect=29%2C32%2C993%2C617&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Red-backed voles may be harboring Alaskapox.</span> <span class="attribution"><a class="source" href="https://ecuador.inaturalist.org/">iNaturalist Ecuador</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc-sa/4.0/">CC BY-NC-SA</a></span></figcaption></figure><p><em>Alaskapox, a virus in the same family as smallpox, cowpox and mpox, <a href="https://abcnews.go.com/Health/wireStory/alaskapox-recent-death-brings-attention-virus-small-animals-107207953">claimed its first fatality</a> in January 2024 when an elderly Alaskan man died of the illness.</em></p>
<p><em>The virus, which was discovered in 2015, had previously resulted in only relatively mild illnesses in the six other people infected by it. So why did the Alaskan man die?</em></p>
<p><em>Raúl Rivas González, a microbiologist at the University of Salamanca in Spain, explains what we know about Alaskapox, what happened to the man in Alaska, and the threat posed by the thousands of similar viruses out there.</em></p>
<h2>What’s the origin of Alaskapox?</h2>
<p>Alaskapox is an orthopox virus <a href="https://doi.org/10.1093%2Fcid%2Fcix219">discovered in 2015</a> in the Fairbanks area of Alaska. </p>
<p>Until the most recent case, there were only six known human infections, which all involved mild illnesses consisting of a localized rash and the swelling of lymph nodes. </p>
<h2>How did the man in Alaska die?</h2>
<p>In mid-September 2023, the man was living on the Kenai Peninsula, south of the city of Anchorage, Alaska, and <a href="https://abcnews.go.com/Health/wireStory/alaskapox-recent-death-brings-attention-virus-small-animals-107207953">undergoing drug treatment for cancer</a>, and so had a suppressed immune system. He noticed a tender red papule – a type of skin lesion – in his right armpit.</p>
<p>Understandably, he was scared and decided to go to the doctor immediately. Over the next six weeks, he made several visits to the primary care center and the local emergency department for clinical evaluation of the lesion.</p>
<p>The case was confusing and the possible infection difficult to identify. He did not respond to antibiotic treatment. A needle biopsy revealed no evidence of malignancy or bacterial infection. The health care providers were puzzled. </p>
<p>After the situation worsened, the man was hospitalized in Anchorage. Eventually, doctors performed an extensive battery of tests and sent a sample to the Centers for Disease Control and Prevention, which determined he had <a href="http://www.doi.org/10.3390/v11080708">Alaskapox</a>.</p>
<p>He was immediately given treatment for the virus, but it was too late and he died at the end of January. Officials <a href="https://epi.alaska.gov/bulletins/docs/b2024_02.pdf">confirmed the cause of death</a> was Alaskapox in February.</p>
<h2>Where do viruses like Alaskapox come from?</h2>
<p>Currently, more than <a href="https://doi.org/10.1128%2Fjcm.00337-22">10,000 species of viruses</a> have been recognized by the International Committee on Taxonomy of Viruses. We know that about 270 of them can infect people. </p>
<p>Some of these viruses have been known for centuries, such as polio and smallpox, while others like Alaskapox have only recently emerged. In fact, viruses constitute about <a href="https://doi.org/10.1098%2Frstb.2011.0354">two-thirds of all new human pathogens</a>. These new viruses differ widely in their risk to human health, ranging from the rare and mild illness caused by the Menangle virus to the <a href="https://covid.cdc.gov/covid-data-tracker/#datatracker-home">devastating public health impact</a> of the virus that causes COVID-19. </p>
<p>Of the viruses known to infect humans, about 80% are naturally occurring in nonhuman hosts, primarily <a href="https://doi.org/10.1016%2Fj.scitotenv.2020.142372">in mammals and birds</a> and, to a lesser extent, in arthropods and other wildlife. </p>
<p>Infectious agents transmitted from animals to humans are estimated to constitute about 60% of known human pathogens and up to <a href="https://doi.org/10.1073/pnas.1919176117">75% of emerging human pathogens</a>. Unfortunately, there is insufficient knowledge about wild animals that may harbor thousands of unknown virus species that could be human pathogens. </p>
<p>The evidence so far indicates that the Alaskapox virus is present in several species of <a href="https://doi.org/10.1093%2Fcid%2Fcix219">small mammals</a>, most notably shrews and the red-backed vole. In other words, Alaskapox is a new example of an infectious disease that can make the leap from animals to humans, a process known as zoonosis. Although available data suggests that the public health impact of Alaskapox virus is limited, it is likely widespread in small mammal populations in Alaska, and other infections in people may not have been diagnosed. </p>
<p>At present, no person-to-person transmission of Alaskapox has been documented. However, because some types of orthopoxviruses can be transmitted by direct contact with skin lesions, it is recommended that people with wounds that are suspected to be caused by Alaskapox keep the affected area covered with a bandage.</p>
<h2>What other orthopoxviruses pose a risk?</h2>
<p>In addition to Alaskapox virus, some other orthopoxviruses have recently been recognized, such as Akhmeta virus and/or Abatino virus, that highlight the possibility of unknown members of this genus with <a href="https://doi.org/10.1056%2FNEJMoa1407647">zoonotic potential</a>. </p>
<p>Other orthopoxviruses with zoonotic potential, such as mpox virus and cowpox virus, are increasingly being reported as a cause of human disease. In fact, the ongoing mpox outbreak that started in May 2022 has resulted in more than <a href="https://www.cdc.gov/poxvirus/mpox/response/2022/index.html">93,000 cases and 177 deaths</a>. This situation may have been facilitated by the discontinuation of routine vaccination against the eradicated human smallpox, as this vaccine gave rise to <a href="https://doi.org/10.1038/s41392-023-01574-6">some degree of population immunity</a> against other orthopoxviruses.</p>
<p>In addition to the above, there are many other orthopoxviruses that infect mammals. Examples are the ectromelia virus that causes mousepox, camelpox, raccoonpox, gerbilpox and skunkpox or some sublineages of vaccinia virus such as rabbitpox and buffalopox. </p>
<p>Poxviruses infect a broad spectrum of hosts, including insects, birds, reptiles and mammals. The wide host range, the wide geographical distribution and the constant global emergence of zoonotic viruses, including new orthopoxviruses, pose a global health threat that requires close monitoring and appropriate preventive measures. </p>
<p>In this situation, I believe the most prudent course of action is to urgently adopt a <a href="https://www.cdc.gov/onehealth/basics/index.html">One Health approach</a> that recognizes that the health of humans, animals, plants and the wider environment are interconnected, and accept that we cannot address human health without also addressing animal and environmental health.</p><img src="https://counter.theconversation.com/content/223470/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Raúl Rivas González 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>Alaskapox was discovered in 2015 and has generally only caused mild illness – until now.Raúl Rivas González, Catedrático de Microbiología. Miembro de la Sociedad Española de Microbiología., Universidad de SalamancaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2222962024-02-05T16:13:03Z2024-02-05T16:13:03ZA new virus-like entity has just been discovered – ‘obelisks’ explained<figure><img src="https://images.theconversation.com/files/573101/original/file-20240202-31-42ohg4.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C8038%2C5354&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/rear-view-male-doctor-taking-bodily-1510584707">Andrey_Popov/Shutterstock</a></span></figcaption></figure><p>Biological entities called obelisks have been hiding – in large numbers – inside the human mouth and gut. These microscopic entities, which were recently discovered by a team at Stanford University, are circular bits of genetic material that contain one or two genes and self-organise into a rod-like shape. </p>
<p>Although the study is still in <a href="https://www.biorxiv.org/content/10.1101/2024.01.20.576352v1">preprint</a> form, meaning that it has not been peer-reviewed, it has already been extensively written about, including in two heavyweight journals: <a href="https://www.nature.com/articles/d41586-024-00266-7">Nature</a> and <a href="https://www.science.org/content/article/it-s-insane-new-viruslike-entities-found-human-gut-microbes">Science</a>.</p>
<p>Let’s delve deeper into the strange world of very tiny “lifeforms”.</p>
<p>In biology, as in physics, things can get weirder and the rules fuzzier as we move through smaller and smaller scales. </p>
<p>Viruses, being unable to replicate without the help of a host, can most generously be considered to be on the edge of what constitutes life. Yet the estimated <a href="https://www.nationalgeographic.com/science/article/factors-allow-viruses-infect-humans-coronavirus">10 nonillion (one followed by 31 zeroes) individual viruses</a> on the planet can be found in every conceivable habitat and, through infecting and manipulating their hosts, have probably affected the evolutionary trajectories of all life. </p>
<p>Peering even further down into the world of minuscule biological entities, are the viroids – tiny scraps of genetic material (DNA-like molecules known as RNA) that cannot make proteins and, unlike viruses, don’t have a protective shell to encase their genome. </p>
<p>Viroids are examples of ribozymes: RNA molecules that may be a distant echo of the very first self-replicating genetic elements from which cellular life emerged. </p>
<p>Viroids can self-cleave (chop up) and re-ligate (stick back together) their genome as part of the replication cycle. And, despite their simplicity, they can cause serious disease in <a href="https://pubmed.ncbi.nlm.nih.gov/33801996/">flowering plants</a>.</p>
<h2>Between a virus and a viroid – perhaps</h2>
<p>The new <a href="https://www.biorxiv.org/content/10.1101/2024.01.20.576352v1.full">preprint</a> describes “viroid-like colonists of human microbiomes”. If “viroid-like” sounds non-committal, that is entirely deliberate. The newly discovered biological entity falls somewhere between viruses and viroids. </p>
<p>In fact, the name obelisks was proposed not only because of their shape, but also to provide wiggle room in case they turn out to be more like RNA plasmids (a different type of genetic element that resides inside bacteria) than either viruses or viroids.</p>
<p>Like viroids, obelisks have a circular single-stranded RNA genome and no protein coat but, like viruses, their genomes contain genes that are predicted to code for proteins. </p>
<p>All obelisks so far described encode a single major protein known as obulin, and many encode a second, smaller obulin. </p>
<p>Obulins bear no evolutionary resemblance, or “homology”, to any other protein found, and there are few clues as to their function. </p>
<p>By analysing existing datasets taken from the gut and mouth of humans as well as other diverse sources, the Stanford team found almost 30,000 distinct obelisk types. </p>
<p>These obelisk genomes have been previously overlooked because they are so dissimilar to anything described previously. The Stanford team found them using a clever bespoke method for searching databases for single-stranded circular RNA molecules to fish out any viroid-like elements. </p>
<p>It is clear from their results that obelisks are not rare. The researchers found them in datasets spanning the globe and in diverse niches. </p>
<p>These elements were detected in around 7% of microbiome datasets from the human gut and 50% of datasets from the mouth. However, whether these datasets provide a true representation of the prevalence and distribution of obelisks is unclear. </p>
<p>Different obelisk types were found in different body sites and in different donors. Long-term data revealed that people can harbour a single obelisk type for around a year. </p>
<p>Obelisks probably rely on microbial host cells to replicate, including those that live inside humans to replicate. Bacteria or fungi are likely hosts, but it is not known which exact species harbour these elements. </p>
<p>However, the researchers provide a critical lead through the analysis by providing strong evidence that a common bacterial component of dental plaque, <em>Streptococcus sanguinis</em>, plays host to a specific obelisk type.</p>
<figure class="align-center ">
<img alt="Illustration of the human gut full of microbes" src="https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=425&fit=crop&dpr=1 754w, https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=425&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/573105/original/file-20240202-29-62uqwp.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=425&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">We might have to re-think the gut microbiome.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/3d-rendered-medical-illustration-microbiome-small-2221001821">SciePro/Shutterstock</a></span>
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<h2>Friend or foe?</h2>
<p>As <em>S sanguinis</em> is easy to grow and experiment on in the laboratory, this will provide a valuable model for understanding the fundamentals of obelisk biology. </p>
<p>This is critical, as nothing is known about the broader evolutionary and ecological significance of obelisks. They may be parasitic and harm host cells, or they may be beneficial. </p>
<p>Hosts may have evolved elaborate defence mechanisms against obelisks, or else actively recruit them to gain some unsuspected advantage. If obelisks change or upset the human microbiome, this may in turn have implications for human health – they may even have therapeutic potential. </p>
<p>Alternatively, obelisks may cause neither harm nor benefit to their microbial host, or to humans. Instead, they may simply exist as stealthy evolutionary passengers, silently and endlessly replicating, like the original “selfish gene”.</p><img src="https://counter.theconversation.com/content/222296/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ed Feil 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>Your mouth and your gut is full of them. But we don’t know if they’re friend or foe.Ed Feil, Professor of Microbial Evolution at The Milner Centre for Evolution, University of BathLicensed as Creative Commons – attribution, no derivatives.tag: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>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1745782729558348212"}"></div></p>
<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">
<figcaption>
<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>
</figcaption>
</figure>
<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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<p>
<em>
<strong>
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>
</strong>
</em>
</p>
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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/2209802024-01-15T20:46:57Z2024-01-15T20:46:57ZRSV, flu and COVID: demystifying the triple epidemic of respiratory viruses<figure><img src="https://images.theconversation.com/files/568892/original/file-20240110-27-k3w5hm.jpg?ixlib=rb-1.1.0&rect=0%2C2%2C995%2C663&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The influenza virus, which causes seasonal flu, is back at its usual rate after a hiatus due to health measures.</span> <span class="attribution"><span class="source">(Shutterstock)</span></span></figcaption></figure><p>Since 2022, a triple epidemic of respiratory viruses — RSV, influenza and SARS-CoV-2 — has been disrupting our daily lives. In addition, the media constantly reminds us of how this is straining emergency departments.</p>
<p>How does the present respiratory virus season differ from seasons during the pre-COVID era?</p>
<p>As a specialist in virus-host interaction, I would like to shed some light on the new dynamics of the respiratory virus season.</p>
<h2>The infamous SARS-CoV-2</h2>
<p>SARS-CoV-2, the instigator of the COVID-19 pandemic, is still with us. Despite limited access to screening tests, analysis of the number of hospital admissions shows that the virus is still going strong.</p>
<p>Québec’s Institut National de Santé Publique counted more than 33,000 hospitalizations in Québec in 2023 affecting all age categories, <a href="https://www.inspq.qc.ca/en/node/29197">including 648 children under the age of nine</a>.</p>
<p>The virus is not seasonal. It has a strikingly efficient capacity to spread through aerosols, especially as we take refuge indoors to escape the cold. The virus currently circulating is actually a mixture of different viruses, known as variants, each of which has the potential to partially evade the immunity an individual has acquired through a previous infection or vaccination.</p>
<h2>Resurgence of seasonal flu</h2>
<p>After a hiatus due to health measures, the influenza virus, which causes seasonal flu, has returned with the same force. It is once again circulating <a href="https://www.cdc.gov/flu/about/viruses/types.htm">in different variants belonging to Types (strains) A and B</a>, although scientists believe that one Type B strain, the <a href="http://doi.org/10.2807/1560-7917.ES.2022.27.39.2200753">Yamagata lineage, has disappeared</a>.</p>
<p>A variant of H1N1 Type A, different from the viruses that caused the 1918 and 2009 pandemics, is now dominant in North America where it is causing an increase in hospital admissions, <a href="https://www.canada.ca/en/public-health/services/publications/diseases-conditions/fluwatch/2023-2024/week-49-december-3-december-9-2023.html">especially among the elderly and young children</a>.</p>
<p>However, we must remain vigilant, as the strain may change within the same season. What could this mean? The target population could change, <a href="https://www.canada.ca/en/public-health/services/publications/diseases-conditions/fluwatch/2018-2019/annual-report.html">as it did in the 2018-2019 season</a>.</p>
<h2>And what about RSV?</h2>
<p>The respiratory syncytial virus (RSV) also appears to be <a href="https://www.canada.ca/en/public-health/services/surveillance/respiratory-virus-detections-canada/2023-2024/week-50-ending-december-16-2023.html">resuming its pre-pandemic transmission levels</a>.</p>
<p>RSV causes bronchiolitis and pneumonia. <a href="https://cps.ca/en/documents/position/bronchiolitis">Bronchiolitis is characterized by the obstruction of the small airways, which can progress to wheezing or respiratory distress</a>.</p>
<p>Virtually all children are infected with RSV before the age of 2, and RSV infection is one of the main causes of hospitalization in young children.</p>
<p>Before the COVID-19 pandemic, there was an average of 2,523 hospitalizations per year in Canada, <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2810133">half of them in children under six months of age and more than a quarter requiring admission to intensive care</a>.</p>
<p>But RSV also severely affects the elderly and adults who are immunocompromised or have existing chronic conditions. RSV shows high levels of severe illness, hospital admissions and in hospital deaths in adults, <a href="https://doi.org/10.1093/infdis/jiad559">figures which are comparable to those for influenza</a>.</p>
<p>Admittedly, although these three viruses are attracting attention, other less publicized respiratory viruses are also circulating, <a href="https://www.canada.ca/en/public-health/services/surveillance/respiratory-virus-detections-canada/2023-2024/week-50-ending-december-16-2023.html">demonstrating a diverse viral environment</a>.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="woman in hospital" src="https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/568438/original/file-20240109-27-z61q6c.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">The continued presence of SARS-CoV-2 means our hospitals can’t catch their breath.</span>
<span class="attribution"><span class="source">(Shutterstock)</span></span>
</figcaption>
</figure>
<h2>SARS-CoV-2 has turned everything upside down</h2>
<p>The presence of SARS-CoV-2 marks the principal difference from the pre-pandemic era, since it is augmenting the burden on an already weakened health-care system. The challenge is amplified by the extremely high transmission capacity of SARS-CoV-2 compared with influenza and RSV, which makes seasonal management much more complex.</p>
<p>Until the SARS-CoV-2 pandemic, the respiratory virus season had a fairly predictable beginning and end that was determined by virus surveillance over the years. Our systems were already struggling to absorb this seasonal increase in patients. But today, the picture has become even more complex with the continuing presence of SARS-CoV-2. And our hospitals, with no time to catch their breath, are struggling to keep up.</p>
<h2>Beyond infection</h2>
<p>The second major difference that should not be overlooked is SARS-CoV-2’s ability to cause widespread health problems well beyond the respiratory system. In addition, it causes long-term consequences after infection, such as post-COVID syndrome (also known as long COVID), which affects millions of people.</p>
<p>The extent of the consequences of infection and reinfection on human health remains uncertain, as does the effectiveness of vaccines in limiting these effects. The SARS-CoV-2 pandemic – with its exceptional transmission levels – has produced a large number of patients available for research. Coupled with unprecedented funding, this has made it possible to undertake research that has never been possible before on a post-viral syndrome.</p>
<p>Of course, the number of people infected with RSV or influenza globally each year does not even come close to the number infected with SARS-CoV-2, even at this stage of the pandemic. However, there is considerable evidence that, in addition to the acute symptoms and mortality associated with influenza and RSV, <a href="https://doi.org/10.1038/s41591-022-01810-6">post-viral conditions also exist</a>, as they do with SARS-CoV-2.</p>
<h2>The importance of vaccines</h2>
<p>The final distinction from the pre-pandemic period is the arrival of RSV vaccines. In Canada, the Arexvy vaccine has been approved for people over 60, and the Abrysvo vaccine was also approved for pregnant women, providing immunity to children from birth. However, these two vaccines have not yet been officially recommended. We are still waiting for a vaccine to be made available for children. The trio of vaccines against COVID-19, influenza and RSV will certainly help to reduce the severe symptoms associated with respiratory virus infections in the coming seasons.</p>
<p>However, our primary objective must be to reduce the incidence of respiratory virus infections. Despite vaccination, we can expect the mortality and morbidity associated with these infections to increase as the population ages.</p>
<p>All three viruses share a common trait — they spread through the air. Their transmission could be reduced by implementing passive strategies aimed at reducing the concentration of aerosols in indoor air.</p><img src="https://counter.theconversation.com/content/220980/count.gif" alt="La Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Nathalie Grandvaux received research funding from the Canadian Institutes of Health Research (CIHR), the Natural Sciences and Engineering Research Council of Canada (NSERC), the Fonds de recherche du Québec - Santé (FRQS), the Canada Foundation for Innovation (CFI), the Fondation du centre hospitalier de l'Université de Montréal, and the Ministère de l'économie et de l'innovation du Québec.</span></em></p>The current triple epidemic of respiratory viruses is affecting all age groups, prompting comparisons with the pre-COVID-19 era.Nathalie Grandvaux, Professeure en biochimie des interactions hôte-virus, Université de MontréalLicensed 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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<p>
<em>
<strong>
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>
<figure class="align-right ">
<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">
<figcaption>
<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>
</figcaption>
</figure>
<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>
<figure>
<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>
</figure>
<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>
<hr>
<p>
<em>
<strong>
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">
<figcaption>
<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>
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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>
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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/2134602023-11-23T19:02:31Z2023-11-23T19:02:31ZDrug resistance may make common infections like thrush untreatable<p><em>Antimicrobial resistance is <a href="https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance">one of the biggest global threats</a> to health, food security and development. This month, The Conversation’s experts <a href="https://theconversation.com/au/topics/the-dangers-of-antibiotic-resistance-146983">explore how we got here and the potential solutions</a>.</em></p>
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<p>We’ve all heard about antibiotic resistance. This happens when bacteria develop strategies to avoid being destroyed by an antibiotic. </p>
<p>The consequences of antibiotic resistance mean an antibiotic previously used to cure bacterial infections no longer works effectively because the bacteria have become resistant to the drug. This means it’s getting harder to cure the infections some bacteria cause.</p>
<p>But unfortunately, it’s only one part of the problem. The same phenomenon is also happening with other causes of infections in humans: fungi, viruses and parasites.</p>
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<strong>
Read more:
<a href="https://theconversation.com/the-rise-and-fall-of-antibiotics-what-would-a-post-antibiotic-world-look-like-213450">The rise and fall of antibiotics. What would a post-antibiotic world look like?</a>
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<p>“Antimicrobial resistance” means the drugs used to treat diseases caused by microbes (bugs that cause infection) no longer work. This occurs with antibacterial agents used against bacteria, antifungal agents used against fungi, anti-parasitic agents used against parasites and antiviral agents used against viruses.</p>
<p>This means a wide range of previously controllable infections are becoming difficult to treat – and may become untreatable. </p>
<h2>Fighting fungi</h2>
<p>Fungi are responsible for a range of infections in humans. Tinea, ringworm and vulvovaginal candidiasis (thrush) are some of the more familiar and common superficial fungal infections. </p>
<p>There are also life-threatening fungal infections such as aspergillosis, cryptococcosis and invasive fungal bloodstream infections including those caused by <em>Candida albicans</em> and <em>Candida auris</em>. </p>
<p>Fungal resistance to antifungal agents is a problem for several reasons. </p>
<p>First, the range of antifungal agents available to treat fungal infections is limited, especially compared to the range of antibiotics available to treat bacterial infections. There are only four broad families of antifungal agents, with a small number of drugs in each category. Antifungal resistance further restricts already limited options.</p>
<p>Life-threatening fungal infections happen less frequently than life-threatening bacterial infections. But they’re rising in frequency, especially among people whose immune systems are compromised, including by <a href="https://7news.com.au/news/qld/first-heart-transplant-patient-to-die-from-fungal-infection-at-brisbanes-prince-charles-hospital-identified-as-mango-hill-gp-muhammad-hussain-c-12551559">organ transplants</a> and chemotherapy or immunotherapy for cancer. The threat of getting a drug-resistant fungal infection makes all of these health interventions riskier.</p>
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<strong>
Read more:
<a href="https://theconversation.com/how-do-candida-auris-and-other-fungi-develop-drug-resistance-a-microbiologist-explains-203495">How do _Candida auris_ and other fungi develop drug resistance? A microbiologist explains</a>
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<p>The greatest <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2017.00735/full">burden of serious fungal disease</a> occurs in places with limited health-care resources available for diagnosing and treating the infections. Even if infections are diagnosed and antifungal treatment is available, antifungal resistance reduces the treatment options that will work.</p>
<p>But even in Australia, common fungal infections are impacted by resistance to antifungal agents. Vulvovaginal candidiasis, known as thrush and caused by <em>Candida</em> species and some closely related fungi, is usually reliably treated by a topical antifungal cream, sometimes supplemented with an oral tablet. However, instances of <a href="https://www.theage.com.au/national/victoria/they-can-t-sit-properly-doctors-treat-growing-number-of-women-with-chronic-thrush-20230913-p5e499.html">drug-resistant thrush</a> are increasing, and new treatments are needed.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1584939012753862657"}"></div></p>
<h2>Targeting viruses</h2>
<p>Even <a href="https://theconversation.com/why-are-there-so-many-drugs-to-kill-bacteria-but-so-few-to-tackle-viruses-137480">fewer antivirals</a> are available than antibacterial and antifungal agents. </p>
<p>Most antimicrobial treatments work by exploiting differences between the microbe causing the infection and the host (us) experiencing the infection. Since viruses use our cells to replicate and cause their infection, it’s difficult to find antiviral treatments that selectively target the virus without damaging us. </p>
<p>With so few antiviral drugs available, any resistance that develops to one of them significantly reduces the treatment options available. </p>
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<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>
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<p>Take COVID, for example. Two antiviral medicines are in widespread use to treat this viral infection: Paxlovid (containing nirmatrelvir and ritonavir) and Lagevrio (molnupiravir). So far, SARS-CoV-2, the virus that causes COVID, has not developed significant resistance to either of these <a href="https://www.cidrap.umn.edu/covid-19/low-levels-resistance-paxlovid-seen-sars-cov-2-isolates">treatments</a>. </p>
<p>But if SARS-CoV-2 develops resistance to either one of them, it halves the treatment options. Subsequently relying on one would likely lead to its increased use, which may heighten the risk that resistance to the second agent will develop, leaving us with no antiviral agents to treat COVID. </p>
<p>The threat of antimicrobial resistance makes our ability to treat serious COVID infections rather precarious.</p>
<h2>Stopping parasites</h2>
<p>Another group of microbes that cause infections in humans are single-celled microbes such as <em>Plasmodium</em>, <em>Giardia</em>, <em>Leishmania</em>, and <em>Trypanosoma</em>. These microbes are sometimes referred to as parasites, and they are becoming increasingly resistant to the very limited range of anti-parasitic agents used to treat the infections they cause. </p>
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<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/antibiotic-resistance-microbiologists-turn-to-new-technologies-in-the-hunt-for-solutions-podcast-217615">Antibiotic resistance: microbiologists turn to new technologies in the hunt for solutions – podcast</a>
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<p>Several <em>Plasmodium</em> species cause malaria and anti-parasitic drugs have been the cornerstone of malaria treatment for decades. But their usefulness has been significantly reduced by the <a href="https://www.mmv.org/our-work/mmvs-pipeline-antimalarial-drugs/antimalarial-drug-resistance">development of resistance</a>. </p>
<p><em>Giardia</em> parasites cause an infection called giardiasis. This can resolve on its own, but it can also cause severe gastrointestinal symptoms such as diarrhea, nausea, and bloating. These microbes have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6207226/">developed resistance</a> to the main treatments and patients infected with drug-resistant parasites can have protracted, unpleasant infections. </p>
<figure class="align-center ">
<img alt="3D illustration of Giardia lamblia protozoan" src="https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/559783/original/file-20231115-19-5oxysw.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"><em>Giardia</em> parasites (illustrated here) cause giardiasis.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/giardia-lamblia-protozoan-causative-agent-giardiasis-1038065005">Shutterstock</a></span>
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<h2>Resistance is a natural consequence</h2>
<p>Treating infections influences microbes’ evolutionary processes. Exposure to drugs that stop or kill them pushes microbes to either evolve or die. The exposure to antimicrobial agents provokes the evolutionary process, selecting for microbes that are resistant and can survive the exposure. </p>
<p>The pressure to evolve, provoked by the antimicrobial treatment, is called “selection pressure”. While most microbes will die, a few will evolve in time to overcome the antimicrobial drugs used against them. </p>
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<p>
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Read more:
<a href="https://theconversation.com/how-do-bacteria-actually-become-resistant-to-antibiotics-213451">How do bacteria actually become resistant to antibiotics?</a>
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</em>
</p>
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<p>The evolutionary process that leads to the emergence of resistance is inevitable. But some things can be done to minimise this and the problems it brings. </p>
<p>Limiting the use of antimicrobial agents is one approach. This means reserving antimicrobial agents for when their use is known to be necessary, rather than using them “just in case”.</p>
<p>Antimicrobial agents are precious resources, holding at bay many infectious diseases that would otherwise sicken and kill millions. It is imperative we do all we can to preserve the effectiveness of those that remain, and give ourselves more options by working to discover and develop new ones.</p>
<hr>
<p><em>Read the other articles in The Conversation’s series on the dangers of antibiotic resistance <a href="https://theconversation.com/au/topics/the-dangers-of-antibiotic-resistance-146983">here</a>.</em></p><img src="https://counter.theconversation.com/content/213460/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Christine Carson receives funding from state and federal funding agencies, and the CUREator program, a national biotechnology incubator delivered by Brandon BioCatalyst. She has a commercial interest in companies developing diagnostic tests and preventing viral infections.</span></em></p>We’ve all heard of antibiotic resistance. The same thing is happening with other causes of infections in humans: fungi, viruses and parasites. This is making thrush and other infections hard to treat.Christine Carson, Senior Research Fellow, School of Medicine, The University of Western AustraliaLicensed 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>
<figure>
<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>
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<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>
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<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>
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<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>
<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 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>
</figcaption>
</figure>
<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/2164832023-10-27T14:09:00Z2023-10-27T14:09:00ZChad’s first dengue fever outbreak: what you should know<p><em>Chad has <a href="https://www.cidrap.umn.edu/dengue/chad-reports-its-first-dengue-outbreak">reported</a> its first dengue outbreak, according to the World Health Organization (WHO). The country’s health ministry declared an outbreak on 15 August and so far 1,342 suspected cases have been reported, 41 of them confirmed in the laboratory. One death was reported among the patients with lab-confirmed cases. The outbreak started in Ouaddaï province in eastern Chad, currently the outbreak epicentre. Illnesses have also been reported in three other provinces. Godfred Akoto Boafo spoke to medical entomologist Eunice Anyango Owino about the disease.</em></p>
<h2>What causes dengue fever and how does it affect people?</h2>
<p><a href="https://www.who.int/news-room/fact-sheets/detail/dengue-and-severe-dengue">Dengue fever</a> is a mosquito-borne viral disease caused by one of the four dengue virus serotypes. It is primarily transmitted by the <em>Aedes aegypti</em> mosquito and to a lesser extent the <em>Aedes albopictus</em> mosquito, mainly in the tropical and sub-tropical areas of the world. </p>
<p>Infection with one serotype provides long-term immunity to that particular serotype, but not the others. That means that, after recovery, a person can still be infected by the other three serotypes. Serotypes are groups within a single species of microorganisms, such as bacteria or viruses, which share distinctive surface structures.</p>
<p>Most infections produce only mild flu-like illness; 80% of cases are asymptomatic. But getting infected with different serotypes one after the other puts a person at a greater risk of severe dengue, also known as dengue hemorrhagic fever. It is characterised by serious internal bleeding and organ damage, and a sudden drop in blood pressure that causes shock which can be fatal. </p>
<h2>How widespread is it in the Sahel? Why is this first outbreak in Chad significant?</h2>
<p>Dengue fever has been <a href="https://pubmed.ncbi.nlm.nih.gov/37473544/">endemic in Sudan</a>, with outbreaks documented in 2010, 2013, 2017 and 2019. Unfortunately, due to years of political and civil conflicts, the control and response capacity of the public health sector in Sudan has been limited. </p>
<p>The risk of spread in the Sahel region, which includes Niger, Mali and Chad, has always been high. This is because these countries all host the suitable mosquito vectors (<em>Aedes</em>). They also share the same tropical climate with seasonal heavy rains and floods. </p>
<p>To add to the problem, countries like Chad are grappling with a massive influx of refugees and returnees from Sudan who might be carrying the disease. The epicentre of the current outbreak, the <a href="https://www.unocha.org/publications/report/chad/chad-humanitarian-update-june-2023#:%7E:text=Following%20the%20escalation%20of%20conflict%20in%20El%20Geneina,Sudanese%20border%20in%20the%20Ouadda%C3%AF%20province%20of%20Chad">province of Ouaddaï</a> at the eastern border with Sudan, hosts more than 400,000 refugees. </p>
<p>The cities at the border with Sudan are densely populated and have poor sanitation. This provides a favourable environment for the vectors to breed. </p>
<p>In addition, Chad lacks effective disease control programmes. This is its first dengue outbreak. It doesn’t have the necessary public health preparedness and response capacities. So the risk posed by this outbreak is high. </p>
<p>The movement of the <a href="https://www.who.int/emergencies/disease-outbreak-news/item/2019-DON207">returning refugees</a> has the potential to spread the outbreak in Chad and even across the border to other countries in the Sahel, the rest of Africa, and the world at large. </p>
<h2>What treatment is available?</h2>
<p>There’s currently no available treatment for dengue in the world. Timely detection and case management, especially treatment of dehydration and plasma leakage by oral or intravenous rehydration, are key in preventing severe illness and death. </p>
<p>There is an approved dengue vaccine (Dengvaxia) for use in people aged 9-45 years. But for it to be effective they must have had one infection of dengue by any of the four serotype viruses, which must be confirmed by a laboratory test. </p>
<p>The vaccine is given in three doses within 12 months and protects against all the four dengue virus serotypes with an efficacy of 80%. However, its availability in developing countries in Africa isn’t assured, although it has been licensed by several national regulatory authorities. </p>
<p>Apart from the vaccine, the only other guard against dengue fever is prevention of mosquito bites and vector control.</p>
<h2>What is the way forward in controlling the disease?</h2>
<p>More investment should be put on expanding clinical and laboratory capabilities to deal with the disease. Given that this is Chad’s first outbreak, it needs to:</p>
<ul>
<li><p>put in place standard operating procedures for clinical management of suspected and confirmed dengue cases </p></li>
<li><p>expand the capacity for early detection of cases – this could be done by procurement of rapid diagnostic tests and by alerting communities </p></li>
<li><p>strengthen disease surveillance and coordinate the response by actively finding cases. Cases within the community are likely to be underreported as dengue is unknown to the public. Also, clinicians might not be familiar with the disease presentation. It could be confused with other common fevers. </p></li>
<li><p>put in place effective vector control measures, like draining stagnant water around residential areas, cleaning and replenishing water storage containers on a weekly basis, distributing insecticide-treated nets, spraying indoors and using window and door screens.</p></li>
<li><p>strengthen surveillance to assess the vector breeding potential in containers and to monitor insecticide resistance. This is critical for selecting the most effective insecticides. </p></li>
<li><p>make communities aware of the risks of infection and how to protect themselves. Engaged communities can take ownership of the vector control strategy and adopt healthy behaviours. </p></li>
<li><p>strengthen cross-border collaboration. The current outbreak most likely spread from Sudan. The focus should be on prevention and vector control measures in border areas.</p></li>
<li><p>mobilise resources for a national contingency plan for dengue preparedness and response. And seek help from experienced organisations like the WHO.</p></li>
</ul><img src="https://counter.theconversation.com/content/216483/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Eunice Anyango Owino receives funding from National Research Fund, Kenya. </span></em></p>The Sahel region is grappling with an outbreak of the deadly mosquito-borne disease.Eunice Anyango Owino, Medical Entomologist at the School of Biological Sciences, University of NairobiLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2156672023-10-19T11:57:12Z2023-10-19T11:57:12ZBird flu in South Africa: expert explains what’s behind the chicken crisis and what must be done about it<p><em>An outbreak of <a href="https://www.woah.org/en/disease/avian-influenza/">avian flu</a> – a highly contagious viral infection that affects wild birds as well as poultry – <a href="https://www.nicd.ac.za/avian-influenza-outbreak/">has hit poultry farms in South Africa</a>. Two different strains are causing outbreaks in the country – A(H5N1) and influenza A(H7N6). A specialist in poultry health, Shahn Bisschop, answers some questions put to him by The Conversation Africa.</em></p>
<h2>What strain has broken out in South Africa?</h2>
<p>The outbreak caused by a highly pathogenic (HPAI) strain of H7N6 avian influenza is causing the most concern at present. The strain was <a href="https://www.news24.com/fin24/companies/bird-flu-super-infectious-sa-strain-emerges-in-mpumalanga-20230627">first confirmed in chickens</a> near Delmas north of Johannesburg at the beginning of June 2023.</p>
<p>This virus is a novel mutation of a strain which originated from wild birds at or near the location of the original outbreak. </p>
<p>The strain is well-adapted to chickens – it infects them easily and replicates effectively in them, in preference to other avian species – and spreads very easily between birds and farms. An <a href="https://sapa.jshiny.com/jdata/sapa/outbreaklanding/">estimated</a> 10 million have become infected while 6 million died from the H7N6. A further 1.7 million died from H5N1 earlier in the year.</p>
<p>The conventional control measures (collectively known as biosecurity) have been less effective than usual in limiting the spread of the disease. The main measures taken on poultry farms include strictly limiting human and vehicle movement. People entering farms will typically take further measures to limit disease transmission such as showering, changing clothes and disinfecting footwear when moving between different parts of the farm. </p>
<p>Because wild birds are associated with the spread of avian flu, measures are taken to ensure they are completely excluded from all chicken sheds. </p>
<h2>What’s new this time?</h2>
<p>For at least the past nine years, HPAI H5 viruses of the 2.3.4.4 clade <a href="https://www.nature.com/articles/s41421-023-00571-x">have been spread across the globe</a> principally by wild bird migrations and infect a range of avian and mammalian species. The first recorded cases caused by viruses belonging to this clade were reported in South Africa in 2017. A second outbreak occurred in 2020. It was anticipated that the next outbreak would probably also be caused by these viruses and indeed the first reported cases of HPAI in 2023 in the coastal regions were associated with H5 strains.</p>
<p>Local experts are working on the theory that the present outbreak of H7N6 HPAI <a href="https://www.cdc.gov/flu/avianflu/avian-in-birds.htm">was created</a> when a low pathogenicity AI (LPAI) virus circulating without causing disease in wild birds underwent a mutation to become an HPAI strain adapted to causing serious disease in chickens. This mutation occurred locally. </p>
<p>Mutation from LPAI to HPAI has been described in poultry in various parts of the world but was considered less likely than the return of the H5 clade 2.3.4.4 viruses previously encountered.</p>
<h2>What’s in place and what’s missing</h2>
<p>Avian influenza is a “controlled disease”. That means it’s placed under strict government control with the aim of eradication as quickly as possible when outbreaks are detected. All outbreaks on farms are immediately reported to the state veterinary service, which takes responsibility for the disease. </p>
<p>The protocol for HPAI control is that all affected farms are placed under strict quarantine and all surviving birds are destroyed and disposed of as quickly as possible in order to limit the further spread of the disease.</p>
<p>But there are weaknesses in the system. </p>
<p>The biggest is that the state veterinary services don’t have sufficient resources to manage the outbreaks effectively.</p>
<p>Secondly, because the state doesn’t compensate farmers for their losses, they have difficulty getting farmers to comply with orders to cull. This has meant that outbreaks have spread out of control. Infected birds have been moved off infected farms for sale – taking the disease with them.</p>
<p>Farmers in the EU and US are compensated when culling happens. This used to be the case in South Africa but no longer happens.</p>
<p>As a result, South Africa has struggled to contain HPAI outbreaks. In<a href="https://www.nicd.ac.za/wp-content/uploads/2017/06/NICD-Avian-influenza-FAQ_final1-1.pdf"> 2017</a> and <a href="https://rr-africa.woah.org/en/immediate-notifications-in-africa/">2020/21</a> the outbreaks gradually slowed and eventually stopped. </p>
<p>HPAI outbreaks tend to be seasonal. In Europe, they occur principally in winter months. In South Africa, there is a similar but less clear trend to more cases in the winter and fewer in summer. This may be related to reduced viral survival in hotter summer weather.</p>
<h2>Are there new approaches to consider?</h2>
<p>New and innovative thinking is needed to deal with the reality on the ground in South Africa.</p>
<p>One possible solution is the introduction of appropriate vaccines. This would reduce the losses associated with outbreaks and would slow the spread of the disease between farms. Like all vaccines, they can’t prevent birds from becoming infected but they can manage the level of infection and spread. But they can’t eradicate the disease. </p>
<p>But there are limited options in terms of available vaccines. And South Africa would need to ensure that the vaccines registered for use in the country were effective against the local strain. If vaccines are poorly matched to outbreak strains, they won’t be effective.</p>
<p>All of this will take time, even with the best effort of government and industry. </p>
<h2>Does the strain pose a risk to people? What should consumers should be aware of?</h2>
<p>The South African Poultry Association <a href="http://www.poultrydiseases.co.za/750-2/">has made it clear</a> that poultry products are safe for consumption. It has been <a href="https://www.up.ac.za/research-matters/news/post_2991581-up-researchers-weigh-in-on-bird-flu-outbreak">collaborating with the University of Pretoria</a> to make sure poultry products are indeed safe. Together with leading scientists they have sequenced the current field strain of H7 avian influenza virus. In <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10302261/">a recent paper </a> scientists reported that none of the amino acid markers were present that afford the virus the ability to bind to mammalian cells.</p>
<p>This shows that infection of humans with the current virus is highly unlikely.</p><img src="https://counter.theconversation.com/content/215667/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Shahn Bisschop 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>New and innovative thinking is needed to deal with the reality on the ground in South Africa.Shahn Bisschop, Senior lecturer, specialist poultry veterinarian, University of PretoriaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2116512023-10-11T12:29:43Z2023-10-11T12:29:43ZYour immune system makes its own antiviral drug − and it’s likely one of the most ancient<figure><img src="https://images.theconversation.com/files/552140/original/file-20231004-23-x2ljhp.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2309%2C1299&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Blocking viruses from replicating their RNA is one way antivirals work.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/coronavirus-single-rna-strand-microscopic-view-of-royalty-free-image/1275277285">CROCOTHERY/iStock via Getty Images Plus</a></span></figcaption></figure><p>Antiviral drugs are generally considered to be a 20th century invention. But recent research has uncovered an unexpected facet to your immune system: It can <a href="https://doi.org/10.1038/s41586-018-0238-4">synthesize its own antiviral molecules</a> in response to viral infections. </p>
<p><a href="https://lsa.umich.edu/chem/people/faculty/nmarsh.html">My laboratory</a> studies a protein that makes these natural antiviral molecules. Far from a modern human invention, nature evolved cells to make their own “drugs” as the <a href="https://doi.org/10.1074/jbc.REV120.012784">earliest defense against viruses</a>. </p>
<h2>How antivirals work</h2>
<p>Viruses have no independent life cycle – they are <a href="https://theconversation.com/think-like-a-virus-to-understand-why-the-pandemic-isnt-over-yet-and-what-the-us-needs-to-do-to-help-other-countries-161400">completely dependent</a> on the cells they infect to supply all the chemical building blocks needed to replicate themselves. Once inside a cell, the virus hijacks its machinery and turns it into a factory to make hundreds of new viruses.</p>
<p><a href="https://www.britannica.com/science/antiviral-drug">Antiviral drugs</a> are molecules that inactivate proteins essential to the functioning of the virus by exploiting the fundamental differences in the way that cells and viruses replicate. </p>
<p>One key difference between cells and most viruses is how they store their genetic information. All <a href="https://theconversation.com/the-human-genome-project-pieced-together-only-92-of-the-dna-now-scientists-have-finally-filled-in-the-remaining-8-176138">cells use DNA</a> to store their genetic information. DNA is a long, chainlike molecule built from four different chemical building blocks, each representing a different “letter” of the genetic code. These building blocks are connected by chemical bonds in a head-to-tail fashion to produce strings of millions of letters. The order of these letters spells out the genetic blueprint for building a new cell.</p>
<p>Many viruses, however, store their genetic information <a href="https://theconversation.com/were-viruses-around-on-earth-before-living-cells-emerged-a-microbiologist-explains-197880">using RNA</a>. RNA is built from a chain of four chemical letters, just like DNA, but the letters have slightly different molecular structures. RNA is single-stranded, while DNA is double-stranded. Viral genomes are also much smaller than cellular genomes, typically only a few thousand letters long.</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>
<p>When a virus replicates, it makes many copies of its RNA genome using a protein called <a href="https://theconversation.com/messenger-rna-how-it-works-in-nature-and-in-making-vaccines-166975">RNA polymerase</a>. The polymerase starts at one end of the existing RNA chain and “reads” the string of chemical letters one at a time, selecting the appropriate building block and adding it to the growing strand of RNA. This process is repeated until the entire sequence of letters has been copied to form a new RNA chain.</p>
<p>One <a href="https://doi.org/10.1007/978-981-13-9073-9_22">class of antiviral drugs</a> interferes with the RNA copying process in a cunning way. The head-to-tail construction of the RNA chain requires each chemical letter to have two connection points – a head to connect to the previous letter and a tail to allow the following letter to be added on. These antivirals mimic one of the chemical letters but crucially lack the tail connection point. If the RNA polymerase mistakes the drug for the intended chemical letter and adds it to the growing RNA chain, the copying process stops because there is nothing to attach the next letter to. For this reason, this type of antiviral drug is called a chain-terminating inhibitor. </p>
<h2>Viperin as antiviral producer</h2>
<p>Previously, researchers thought that chain-terminating antiviral drugs were strictly a product of human ingenuity, developed from advances in scientific understanding of viral replication. However, the discovery that a protein in your cells <a href="https://doi.org/10.1074/jbc.REV120.012784">named viperin</a> synthesizes a natural chain-terminating antiviral has revealed a new side of your immune system. </p>
<p>Viperin works by chemically removing the tail connection point from one of the four RNA building blocks of a virus’s genome. This converts the building block into a chain-terminating antiviral drug. </p>
<p>This strategy has proved to be highly effective for treating viral infections. For example, the <a href="https://theconversation.com/in-the-fight-against-coronavirus-antivirals-are-as-important-as-a-vaccine-heres-where-the-science-is-up-to-133926">COVID-19 antiviral remdesivir</a> works in this way. A viral RNA polymerase has to join together many thousands of letters to copy a virus’s genome, but an antiviral drug has to fool it only once to derail its copying. An incomplete genome lacks the necessary instructions to make a new virus and becomes useless. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Illustration of Remdesivir blocking a viral RNA polymerase from replicating RNA" src="https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/552129/original/file-20231004-25-kvjat4.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"></a>
<figcaption>
<span class="caption">Remdesivir (red, center) works by blocking a viral RNA polymerase (blue) from replicating RNA (violet and orange).</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/remdesivir-coronavirus-drug-and-target-illustration-royalty-free-image/1307403157">Juan Gaertner/Science Photo Library via Getty Images</a></span>
</figcaption>
</figure>
<p>Moreover, although cells also have their own polymerases, they never replicate RNA like viruses do. This potentially allows chain-terminating antiviral drugs to <a href="https://doi.org/10.1007/978-981-13-9073-9_22">selectively inhibit viral replication</a>, reducing unwanted side effects. </p>
<p>Clearly, viperin does not fully protect against all RNA viruses – otherwise no RNA viruses would make you sick. It seems that some viral RNA polymerases, such as those <a href="https://doi.org/10.1038/s41586-018-0238-4">in poliovirus</a>, have evolved to discriminate against the antiviral molecules that viperin synthesizes and blunt their effect. However, viperin is only one arm of your <a href="https://theconversation.com/explainer-how-the-human-body-first-fights-off-pathogens-80532">immune system</a>, which includes specialized cells and proteins that protect you from infection in other ways.</p>
<h2>Ancient antivirals</h2>
<p>Scientists <a href="https://doi.org/10.1073/pnas.011593298">discovered viperin</a> about 20 years ago while searching for genes that turn on in response to viral infections. However, figuring out what viperin actually does proved very challenging. </p>
<p>Viperin’s function was particularly puzzling because it resembles an ancient group of proteins called <a href="https://doi.org/10.1021/cr4004709">radical SAM enzymes</a> that are usually found in bacteria and molds. Notably, radical SAM enzymes are extremely rare in animals. Exposure to air rapidly inactivates them, and researchers thought they likely didn’t work in people. It’s still unclear how viperin avoids inactivation.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram showing structure of viperin without (left) and with (right) an antiviral bound in its center. The structure with the antiviral is more tightly wound in its center." src="https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=228&fit=crop&dpr=1 600w, https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=228&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=228&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=287&fit=crop&dpr=1 754w, https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=287&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/551896/original/file-20231003-23-yg2y0k.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=287&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 illustration shows the structure of viperin without (left) and with (right) an antiviral bound in its center.</span>
<span class="attribution"><a class="source" href="https://doi.org/10.1074/jbc.REV120.012784">Soumi Ghosh and Neil Marsh/Journal of Biological Chemistry</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>Researchers were <a href="https://doi.org/10.1038/s41586-018-0238-4">clued in to viperin’s function</a> when they noticed that the gene coding for viperin is next to a gene involved in synthesizing one of RNA’s building blocks. This observation led them to examine whether viperin might modify this RNA building block. </p>
<p>Following this discovery, researchers identified <a href="https://doi.org/10.1038/s41586-020-2762-2">viperinlike proteins</a> across all kingdoms of life, from ancient bacteria to modern plants and animals. This meant that viperin is a very ancient protein that evolved early in life, probably well before the advent of multicellular organisms – because even <a href="https://theconversation.com/viruses-are-both-the-villains-and-heroes-of-life-as-we-know-it-169131">bacteria must fight viral infections</a>. </p>
<p>As more complex life forms evolved, viperin was retained and integrated into the complex immune systems of modern animals. Thus, this most recently discovered arm of your immune system’s defenses against viruses is <a href="https://doi.org/10.1074/jbc.REV120.012784">likely the most ancient</a>.</p><img src="https://counter.theconversation.com/content/211651/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Neil Marsh receives funding from the National Institute of General Medical Sciences to support his laboratory's work on viperin. </span></em></p>The human body has been making antivirals for eons, long before scientists did. A protein in your cells called viperin produces molecules that work similarly to the COVID-19 antiviral remdesivir.Neil Marsh, Professor of Chemistry and Biological Chemistry, University of MichiganLicensed 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>
<hr>
<p>
<em>
<strong>
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>
</strong>
</em>
</p>
<hr>
<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/2108792023-08-02T22:51:06Z2023-08-02T22:51:06ZDoes picking your nose really increase your risk of COVID?<figure><img src="https://images.theconversation.com/files/540914/original/file-20230802-26619-e8ybza.jpg?ixlib=rb-1.1.0&rect=1%2C0%2C997%2C666&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-man-picking-his-nose-167161349">Shutterstock</a></span></figcaption></figure><p>Picking your nose is linked to an increased risk of COVID, according to a <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0288352">study</a> out today.</p>
<p>The study was conducted in health workers. This raises two main questions.</p>
<p>One, were these health workers <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7588529/">washing</a> <a href="https://www.safetyandquality.gov.au/our-work/infection-prevention-and-control/national-hand-hygiene-initiative/what-hand-hygiene/5-moments-hand-hygiene">their hands</a> at work? Two, what does this study mean for the rest of us nose pickers? </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/when-you-pick-your-nose-youre-jamming-germs-and-contaminants-up-there-too-3-scientists-on-how-to-deal-with-your-boogers-185052">When you pick your nose, you're jamming germs and contaminants up there too. 3 scientists on how to deal with your boogers</a>
</strong>
</em>
</p>
<hr>
<h2>What did the study find?</h2>
<p>Some 219 Dutch health workers were monitored for COVID infection. They had regular antibody testing, which tells us if they had been exposed to SARS-CoV-2, the virus that causes COVID. They also reported the results of their own COVID tests.</p>
<p>Some 12-18 months later, the health workers were asked about their nose picking habits, and exposure to COVID via symptomatic workmates or from contacts outside work.</p>
<p>Just over 17% of health workers who reported picking their nose caught COVID versus about 6% of those who did not report nose picking.</p>
<p>At first glance, it might appear feasible that people who pick their noses would be at increased risk of contracting COVID.</p>
<p>That’s because COVID infection relies on the SARS-CoV-2 virus coming into contact with mucous membranes that line the respiratory system, including those in the nose. </p>
<p>So if someone touches a contaminated object or hand, then sticks their finger up their nose, this so-called fomite transmission can occur. </p>
<p>But the risk is comparatively low. The United States Centers for Disease Control <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/science-and-research/surface-transmission.html">estimates</a> about one in 10,000 contacts with a contaminated surface results in SARS-CoV-2 transmission.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/how-clean-is-your-hospital-room-to-reduce-the-spread-of-infections-it-could-probably-be-cleaner-122185">How clean is your hospital room? To reduce the spread of infections, it could probably be cleaner</a>
</strong>
</em>
</p>
<hr>
<h2>Hang on a minute</h2>
<p>But there are some odd results. For example, people who picked their noses only monthly had a higher chance of infection than daily nose pickers. Logically, you would expect the daily nose pickers to have a higher risk of infection due to more transmission opportunities.</p>
<p>There were also several aspects of how the study was designed that may have influenced the results.</p>
<p>Just over half of the people approached to participate in the study actually did so, which may cause <a href="https://www.iwh.on.ca/what-researchers-mean-by/selection-bias#">selection bias</a>. This is where people who choose to participate may differ in some key characteristic from those who don’t. These different characteristics can be “<a href="https://www.sciencedirect.com/topics/nursing-and-health-professions/confounding-variable">confounders</a>” that influence the results.</p>
<p>This was a cohort study, which followed a defined group of people for a set time and asked them questions about their habits and exposure. This study design may also be subject to bias.</p>
<p>That’s because people tend to answer in ways that are <a href="https://www.ajan.com.au/archive/Vol25/Vol_25-4_vandeMortel.pdf">socially desirable</a>, even in anonymous surveys. They tend to under-report behaviours seen as socially unacceptable (such as binge drinking); they over-report those that are socially acceptable.</p>
<p>This study did not control for this type of bias. So we cannot say for certain if someone’s report of whether and how often they picked their nose is a true reflection of what actually happened.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Health worker wearing surgical mask, scrubs and gloves outside carrying folder or clipboard" src="https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/540705/original/file-20230802-17-b2qkwo.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">How often do you pick your nose? Your answer may not be accurate.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-female-ems-key-worker-doctor-1844975320">Shutterstock</a></span>
</figcaption>
</figure>
<p>People in the study may also have had trouble correctly remembering past behaviour (picking their nose) or exposures (to symptomatic people with COVID). The long time lag between when the infection data was collected and the retrospective survey increases the risk of recall error.</p>
<p>There is also some level of “guestimating” in the study, particularly when it comes to the risk of COVID exposure. Health workers were asked to note their contact with symptomatic people or working with COVID patients. But we can’t say if these were real “exposures”. That’s because people may not have symptoms and still have COVID (this would have under-estimated their exposure risk). Alternatively, COVID patients may not be that infectious if they don’t shed much virus (which may have over-estimated the COVID risk).</p>
<p>Then, it appears the analysis did not control for gender. This is potentially an issue as female health workers tend to be <a href="https://pubmed.ncbi.nlm.nih.gov/11743487/">better</a> at following hand hygiene guidelines. The study reported a higher rate of nose picking in males and doctors, and males and <a href="https://www.australiancriticalcare.com/article/S1036-7314(00)70630-8/pdf">doctors</a> are also worse at hand hygiene.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Surgeon washing hands in hospital" src="https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=285&fit=crop&dpr=1 600w, https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=285&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=285&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=358&fit=crop&dpr=1 754w, https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=358&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/540700/original/file-20230802-15-ma6m83.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=358&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 often did health workers wash their hands? The study didn’t say.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/surgeon-hospital-washing-thorouughly-his-hands-1155417787">Shutterstock</a></span>
</figcaption>
</figure>
<p>So the nose pickers may also be worse at sanitising their hands. In other words, we don’t know if nose picking is the reason for the reported increased risk of COVID, the lack of hand hygiene, or both.</p>
<p>Another way of saying this is the researchers reported a <em>correlation</em> between nose picking and an increased risk of COVID. We cannot say one <em>causes</em> the other or if additional factors are involved.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/does-picking-your-nose-really-increase-your-risk-of-dementia-193463">Does picking your nose really increase your risk of dementia?</a>
</strong>
</em>
</p>
<hr>
<h2>So, what now?</h2>
<p>Given the above limitations, the study conclusions seem overly confident. Overall, the risk of SARS-CoV-2 transmission via nose picking is probably comparatively low, particularly for the general public who are not working in high COVID environments. </p>
<p>But you can definitely decrease your risk through good hand hygiene (and using a tissue that you dispose of afterwards).</p>
<p>Better still, avoid inhaling airborne viral particles, which is the <a href="https://www.cdc.gov/coronavirus/2019-ncov/more/science-and-research/surface-transmission.html">most common</a> mode of transmission of SARS-CoV-2. Wear a good fitting mask or respirator in public, particularly in poorly ventilated or crowded inside spaces.</p><img src="https://counter.theconversation.com/content/210879/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Thea van de Mortel teaches into the Griffith University Master of Infection Prevention and Control program. </span></em></p>Health workers who picked their noses were more likely to contract COVID, according to a new study. But here’s what the study means for the rest of us.Thea van de Mortel, Professor, Nursing, School of Nursing and Midwifery, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2070232023-07-28T02:14:53Z2023-07-28T02:14:53ZWhat happens in our body when we encounter and fight off a virus like the flu, SARS-CoV-2 or RSV?<figure><img src="https://images.theconversation.com/files/539186/original/file-20230725-25-dio99v.jpg?ixlib=rb-1.1.0&rect=188%2C32%2C5275%2C3514&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-man-coughing-covering-mouth-tissue-1424228762">Shutterstock</a></span></figcaption></figure><p><a href="https://www.labcorp.com/coronavirus-disease-covid-19/covid-news-education/covid-19-vs-flu-vs-rsv-how-tell-difference">Respiratory viruses</a> like influenza virus (flu), SARS-CoV-2 (which causes COVID) and respiratory syncytial virus (RSV) can make us sick by infecting our respiratory system, including the nose, upper airways and lungs. </p>
<p>They spread from person to person through respiratory droplets when someone coughs, sneezes, or talks and can cause death in serious cases. </p>
<p>But what happens in our body when we first encounter these viruses? Our immune system uses a number of strategies to fight off viral infections. Let’s look at how it does this. </p>
<h2>First line of defence</h2>
<p>When we encounter respiratory viruses, the <a href="https://www.sciencedirect.com/science/article/pii/S193131281600038X?via%3Dihub/">first line of defence</a> is the physical and chemical barriers in our nose, upper airways, and lungs. Barriers like the mucus lining and hair-like structures on the surface of cells, work together to trap and remove viruses before they can reach deeper into our respiratory system. </p>
<p>Our defence also includes our behaviours such as coughing or sneezing. When we blow our nose, the mucus, viruses, and any other pathogens that are caught within it are expelled. </p>
<p>But sometimes, viruses manage to evade these initial barriers and sneak into our respiratory system. This activates the cells of our innate immune system. </p>
<figure class="align-center ">
<img alt="Woman sits on a train holding a tissue" src="https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539184/original/file-20230725-27-mqxwrk.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">Sneezing and blowing our nose can help expel the virus.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/portrait-young-attractive-woman-look-on-1644508063">Shutterstock</a></span>
</figcaption>
</figure>
<h2>Patrolling for potential invaders</h2>
<p>While our acquired immune system develops over time, our innate immune system is present at birth. It generates “non-specific” immunity by identifying what’s foreign. The cells of innate immunity act like a patrol system, searching for any invaders. These innate cells patrol almost every part of our body, from our skin to our nose, lungs and even internal organs. </p>
<p>Our respiratory system has different type of innate cells such – as macrophages, neutrophils and natural killer cells – which patrol in our body looking for intruders. If they recognise anything foreign, in this case a virus, they will initiate an attack response. </p>
<p>Each cell type plays a slightly different role. Macrophages, for example, will not only engulf and digest viruses (phagocytosis) but also release a cocktail of different molecules (cytokines) that will warn and recruit other cells to <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/cmi.12580">fight against the danger</a>. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/explainer-how-does-the-immune-system-learn-37285">Explainer: how does the immune system learn?</a>
</strong>
</em>
</p>
<hr>
<p>In the meantime, natural killer cells, aptly named, attack infected cells, and stop viruses from multiplying and <a href="https://www.nature.com/articles/s41577-021-00558-3">invading our body further</a>. </p>
<p>Natural killer cells also promote inflammation, a <a href="https://www.hindawi.com/journals/jir/2018/1467538/">crucial part of the immune response</a>. It helps to recruit more immune cells to the site of infection, enhances blood flow, and increases the permeability of blood vessels, allowing immune cells to reach the infected tissues.
At this stage, our immune system is fighting a war against viruses and the result can cause inflammation, fevers, coughs and congestion. </p>
<h2>Launching a specific attack</h2>
<p>As the innate immune response begins, another branch of the immune system called the adaptive immune system is <a href="https://www.ncbi.nlm.nih.gov/books/NBK21070/">activated</a>. </p>
<p>The adaptive immune system is more specific than the innate immune system, and it decides on the correct tools and strategy to fight off the viral invaders. This system plays a vital role in eliminating the virus and providing long-term protection against future infections. </p>
<p>Specialised cells called T cells and B cells are key players in acquired immunity. </p>
<p>T cells (specifically, helper T cells and cytotoxic T cells) recognise viral proteins on the surface of infected cells:</p>
<ul>
<li><p>helper T cells release molecules that <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764486/">further activate immune cells</a></p></li>
<li><p>cytotoxic T cells directly kill infected cells with a very great precision, <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2018.00678/full">avoiding any healthy cells around</a>. </p></li>
</ul>
<p>B cells produce antibodies, which are proteins that can bind to viruses, neutralise them, and mark them for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247032/">destruction by other immune cells</a>. </p>
<p>B cells are a critical part of memory in our immune system. They will remember what happened and won’t forget for years. When the same virus attacks again, B cells will be ready to fight it off and will neutralise it faster and better. </p>
<p>Thanks to the adaptive immune system, vaccines for respiratory viruses such as the COVID mRNA vaccine keep us protected from <a href="https://www.health.gov.au/our-work/covid-19-vaccines/our-vaccines/how-they-work">being sick or severely ill</a>. However, if the same virus became mutated, our immune system will act as if it was a new virus and will have to fight in a war again. </p>
<figure class="align-center ">
<img alt="Nurse puts bandaid on patient's arm after a vaccination" src="https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539187/original/file-20230725-16-bkrqq.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">Vaccines help us generate an immune response to viruses we’re immunised against.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/90ejoVTj2-M">CDC/Unsplash</a></span>
</figcaption>
</figure>
<h2>Neutralising the threat</h2>
<p>As the immune response progresses, the combined efforts of the innate and adaptive immune systems helps control the virus. Infected cells are cleared, and the virus is neutralised and eliminated from the body. </p>
<p>As the infection subsides, symptoms gradually improve, and we begin to feel better and to recover. </p>
<p>But recovery varies depending on the specific virus and us as individuals. Some respiratory viruses, like rhinoviruses which cause the common cold, may cause relatively mild symptoms and a quick recovery. Others, like the flu, SARS-CoV-2 or severe cases of RSV, may lead to more severe symptoms and a longer recovery time. </p>
<p>Some viruses are very strong and too fast sometimes so that our immune system does not have the time to develop a proper immune response to fight them off. </p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/ive-had-covid-and-am-constantly-getting-colds-did-covid-harm-my-immune-system-am-i-now-at-risk-of-other-infectious-diseases-188899">I've had COVID and am constantly getting colds. Did COVID harm my immune system? Am I now at risk of other infectious diseases?</a>
</strong>
</em>
</p>
<hr>
<img src="https://counter.theconversation.com/content/207023/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 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>COVID, the flu and RSV spread from person to person through respiratory droplets when someone coughs, sneezes or talks. Here’s how our body fights them off.Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityWesley Freppel, Research Fellow, Institute for Glycomics, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2097952023-07-27T20:11:18Z2023-07-27T20:11:18ZAncient pathogens released from melting ice could wreak havoc on the world, new analysis reveals<figure><img src="https://images.theconversation.com/files/539710/original/file-20230727-23-jtkhdm.jpeg?ixlib=rb-1.1.0&rect=0%2C66%2C4025%2C2565&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>Science fiction is rife with fanciful tales of deadly organisms emerging from the ice and wreaking havoc on unsuspecting human victims. </p>
<p>From <a href="https://www.imdb.com/title/tt0084787/">shape-shifting aliens</a> in Antarctica, to super-parasites emerging from a <a href="https://www.imdb.com/title/tt1235448/">thawing woolly mammoth</a> in Siberia, to exposed <a href="https://www.nytimes.com/2021/05/20/books/review/jim-shepard-phase-six.html">permafrost in Greenland</a> causing a viral pandemic – the concept is marvellous plot fodder.</p>
<p>But just how far-fetched is it? Could pathogens that were once common on Earth – but frozen for millennia in glaciers, ice caps and <a href="https://climate.mit.edu/explainers/permafrost">permafrost</a> – emerge from the melting ice to lay waste to modern ecosystems? The potential is, in fact, quite real. </p>
<h2>Dangers lying in wait</h2>
<p>In 2003, <a href="https://ami-journals.onlinelibrary.wiley.com/doi/abs/10.1046/j.1462-2920.2003.00422.x">bacteria were revived</a> from samples taken from the bottom of an ice core drilled into an <a href="https://byrd.osu.edu/research/groups/ice-core-paleoclimatology/projects/china/guliya">ice cap</a> on the <a href="https://goo.gl/maps/zjN3NVk8TAb6GrxZ9">Qinghai-Tibetan plateau</a>. The ice at that depth was more than 750,000 years old. </p>
<p>In 2014, a giant “zombie” <em>Pithovirus sibericum</em> virus was <a href="https://www.pnas.org/doi/abs/10.1073/pnas.1320670111">revived from</a> 30,000-year-old Siberian permafrost.</p>
<p>And in 2016, an outbreak of <a href="https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/anthrax">anthrax</a> (a disease caused by the bacterium <em>Bacillus anthracis</em>) <a href="https://goo.gl/maps/fjV8u2mRbbC7UoAs5">in western Siberia</a> was attributed to the rapid <a href="https://link.springer.com/article/10.1007/s10393-021-01549-5">thawing of <em>B. anthracis</em> spores</a> in permafrost. It killed thousands of reindeer and affected dozens of people.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=395&fit=crop&dpr=1 600w, https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=395&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=395&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=496&fit=crop&dpr=1 754w, https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=496&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/537599/original/file-20230716-126451-ymm8xc.jpeg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=496&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption"><em>Bacillus anthracis</em> is a soil bacterium that causes anthrax.</span>
<span class="attribution"><span class="source">William A. Clark/USCDCP</span></span>
</figcaption>
</figure>
<p>More recently, scientists found <a href="https://royalsocietypublishing.org/doi/10.1098/rspb.2022.1073">remarkable genetic compatibility</a> between viruses isolated from lake sediments in the high Arctic and potential living hosts.</p>
<p>Earth’s climate is warming at a <a href="https://theconversation.com/it-can-be-done-it-must-be-done-ipcc-delivers-definitive-report-on-climate-change-and-where-to-now-201763">spectacular rate</a>, and up to four times faster <a href="https://www.nature.com/articles/s43247-022-00498-3">in colder regions</a> such as the Arctic. Estimates suggest we can expect <a href="https://ami-journals.onlinelibrary.wiley.com/doi/10.1111/j.1462-2920.2012.02876.x">four sextillion</a> (4,000,000,000,000,000,000,000) microorganisms to be released from ice melt each year. This is about the same as the estimated number of stars <a href="https://www.esa.int/Science_Exploration/Space_Science/Herschel/How_many_stars_are_there_in_the_Universe">in the universe</a>.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/for-110-years-climate-change-has-been-in-the-news-are-we-finally-ready-to-listen-188646">For 110 years, climate change has been in the news. Are we finally ready to listen?</a>
</strong>
</em>
</p>
<hr>
<p>However, despite the unfathomably large number of microorganisms being released from melting ice (including pathogens that can potentially infect modern species), no one has been able to estimate the risk this poses to modern ecosystems.</p>
<p>In <a href="http://doi.org/10.1371/journal.pcbi.1011268">a new study</a> published today in the journal PLOS Computational Biology, we calculated the ecological risks posed by the release of unpredictable ancient viruses.</p>
<p>Our simulations show that 1% of simulated releases of just one dormant pathogen could cause major environmental damage and the widespread loss of host organisms around the world.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/537499/original/file-20230714-15-iyqll0.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">Melt water carving a glacier in the Himalayas of India.</span>
<span class="attribution"><span class="source">Sharada Prasad</span></span>
</figcaption>
</figure>
<h2>Digital worlds</h2>
<p>We used a software called <a href="https://alife.org/encyclopedia/digital-evolution/avida/">Avida</a> to run experiments that simulated the release of one type of ancient pathogen into modern biological communities. </p>
<p>We then measured the impacts of this invading pathogen on the diversity of modern host bacteria in thousands of simulations, and compared these to simulations where no invasion occurred.</p>
<p>The invading pathogens often survived and evolved in the simulated modern world. About 3% of the time the pathogen became dominant in the new environment, in which case they were very likely to cause losses to modern host diversity. </p>
<p>In the worst- (but still entirely plausible) case scenario, the invasion reduced the size of its host community by 30% when compared to controls.</p>
<p>The risk from this small fraction of pathogens might seem small, but keep in mind these are the results of releasing just one particular pathogen in simulated environments. With the sheer number of ancient microbes being released in the real world, such outbreaks represent a substantial danger.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/melting-ice-leaves-polar-ecosystems-out-in-the-sun-19807">Melting ice leaves polar ecosystems out in the sun</a>
</strong>
</em>
</p>
<hr>
<h2>Extinction and disease</h2>
<p>Our findings suggest this unpredictable threat which has so far been confined to science fiction could become a powerful driver of ecological change. </p>
<p>While we didn’t model the potential risk to humans, the fact that “time-travelling” pathogens could become established and severely degrade a host community is already worrisome.</p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/537596/original/file-20230716-122897-5fkiun.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">Drilling ice cores in Greenland.</span>
<span class="attribution"><span class="source">Helle Astrid Kjær</span></span>
</figcaption>
</figure>
<p>We highlight yet another source of potential species extinction in the modern era – one which even our <a href="https://theconversation.com/children-born-today-will-see-literally-thousands-of-animals-disappear-in-their-lifetime-as-global-food-webs-collapse-196286">worst-case extinction models</a> do not include. As a society, we need to understand the potential risks so we can prepare for them.</p>
<p>Notable viruses such as <a href="https://www.sciencedirect.com/science/article/pii/S0092867421009910">SARS-CoV-2</a>, <a href="https://www.science.org/doi/full/10.1126/science.1259657">Ebola</a> and <a href="https://perspectivesinmedicine.cshlp.org/content/1/1/a006841">HIV</a> were likely transmitted to humans via contact with other animal hosts. So it is <a href="https://www.huffpost.com/entry/ice-caps-melt-prehistoric_b_9805334">plausible</a> that a once ice-bound virus could enter the human population via a <a href="https://theconversation.com/how-do-viruses-mutate-and-jump-species-and-why-are-spillovers-becoming-more-common-134656">zoonotic pathway</a>.</p>
<p>While the likelihood of a pathogen emerging from melting ice and causing catastrophic extinctions is low, our results show this is no longer a fantasy for which we shouldn’t prepare.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=300&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=300&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=300&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=377&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=377&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539709/original/file-20230727-25-ftjegw.gif?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=377&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">They may only be microscopic – and far from the giant flesh-eating bugs you’ll see in sci-fi films – but the risks posed by pathogens shouldn’t be underestimated.</span>
<span class="attribution"><a class="source" href="https://cloud.blender.org/p/gallery/629f23f908e12d4ff15241d3">Giovanni Strona, 2023 (based on previous work by Oksana Dobrovolska)</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure><img src="https://counter.theconversation.com/content/209795/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Corey J. A. Bradshaw receives funding from the Australian Research Council.</span></em></p><p class="fine-print"><em><span>Giovanni Strona 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>Researchers simulated thousands of scenarios of an ancient pathogen being released into modern ecosystems. In the worst cases, up to one-third of host species were destroyed.Corey J. A. Bradshaw, Matthew Flinders Professor of Global Ecology and Models Theme Leader for the ARC Centre of Excellence for Australian Biodiversity and Heritage, Flinders UniversityGiovanni Strona, Doctoral program supervisor, University of HelsinkiLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2088552023-07-26T00:32:56Z2023-07-26T00:32:56ZRSV is everywhere right now. What parents need to know about respiratory syncytial virus<figure><img src="https://images.theconversation.com/files/538668/original/file-20230721-21-8jb0lp.jpg?ixlib=rb-1.1.0&rect=1%2C4%2C997%2C661&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/newborn-baby-weakened-bronchitis-getting-oxygen-1022883532">Shutterstock</a></span></figcaption></figure><p>This winter, we’re having to get our heads around another respiratory virus – RSV.</p>
<p>It’s less well known than COVID or flu, but it’s also responsible for unplanned visits to the GP or emergency department, and days off school, childcare and work.</p>
<p>It’s the <a href="https://pubmed.ncbi.nlm.nih.gov/31383776/">most common</a> cause of hospitalisation in infants. Most children have at least one RSV infection by the age of three years and yet, many Australians have not heard of RSV or know little about this potentially serious winter virus.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/mondays-medical-myth-you-can-catch-a-cold-by-getting-cold-2488">Monday's medical myth: you can catch a cold by getting cold</a>
</strong>
</em>
</p>
<hr>
<h2>What is RSV?</h2>
<p>RSV stands for respiratory syncytial (pronounced sin-CITY-al) virus. This common respiratory virus usually causes a mild cold with symptoms such as a fever, runny nose, coughing, decreased appetite and a wheeze. </p>
<p>Adults can be infected with RSV but usually recover in a few days.</p>
<p>But in young babies RSV can cause more severe respiratory illnesses such as <a href="https://www.rch.org.au/kidsinfo/fact_sheets/pneumonia/">pneumonia</a> or <a href="https://www.rch.org.au/kidsinfo/fact_sheets/bronchiolitis/">bronchiolitis</a>. These cause babies to breathe rapidly, stop breathing for a few seconds (apnoeas) and/or feed poorly. RSV in infancy can also potentially affect a child’s long-term health, increasing their risk of asthma, wheezing and allergies. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1676938514951462912"}"></div></p>
<p>In Australia, a wave of RSV infections typically begins in late autumn (April-May) and peaks in June-July. Cases are <a href="https://nindss.health.gov.au/pbi-dashboard/">starting to decline</a> in Australia now.</p>
<p>Because health staff have to report cases of RSV, we can keep track of <a href="https://nindss.health.gov.au/pbi-dashboard/">known cases</a>. But we suspect most go unreported as they are mild and/or doctors don’t always test for the virus.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/heard-of-kindy-flu-theres-no-such-thing-but-kids-are-at-risk-this-flu-season-for-one-simple-reason-207825">Heard of 'kindy flu'? There's no such thing. But kids are at risk this flu season for one simple reason</a>
</strong>
</em>
</p>
<hr>
<h2>Who’s most at risk?</h2>
<p>Both young and old people are most at risk of severe disease. </p>
<p>For children, those <a href="https://adc.bmj.com/content/107/4/359.long">most at risk</a> of severe disease include babies under two months old, premature infants, those with other medical conditions, or ones infected with another virus at the same time. First Nations children are <a href="https://pubmed.ncbi.nlm.nih.gov/31066061/">three to six times</a> more likely to be hospitalised with bronchiolitis caused by RSV than non-First Nations children.</p>
<p>Otherwise healthy children under 12 months old (usually under six months old) are the ones most often admitted to hospital. Of children admitted to hospital, <a href="https://pubmed.ncbi.nlm.nih.gov/35168504/">about a quarter</a> (26%) will be admitted to intensive care.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&rect=4%2C0%2C994%2C667&q=45&auto=format&w=1000&fit=clip"><img alt="Male toddler with oxygen mask over face in hospital bed" src="https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&rect=4%2C0%2C994%2C667&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/538662/original/file-20230721-28237-d8ek9e.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">Young children and the elderly are most at risk.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/2-years-old-asian-toddler-boy-1163046754">Shutterstock</a></span>
</figcaption>
</figure>
<h2>Why are we seeing so many cases now?</h2>
<p>RSV is spread via coughing and sneezing so it’s easy to see how the virus can spread among children inside during winter months.</p>
<p>But measures earlier in the COVID pandemic limited the spread of RSV.</p>
<p>There was very little RSV circulating in 2020 during the harshest lockdowns. However, in New South Wales and Western Australia (in late 2020) and in Victoria (early 2021) there was an <a href="https://www.nature.com/articles/s41467-022-30485-3">out-of-season re-emergence</a> of RSV, overwhelming hospitals and health-care facilities.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1531461682307821570"}"></div></p>
<p>In 2022, RSV settled back into the usual winter peak. However, many states are experiencing a winter surge in cases and hospitalisations attributed to it this year – bigger than before the pandemic.</p>
<p>This may relate to <a href="https://www.health.gov.au/diseases/respiratory-syncytial-virus-rsv-infection">new reporting requirements</a> for RSV and more testing for it.</p>
<p>However, reduced immunity in young infants due to lower maternal and infant exposure may have contributed to the record number of cases.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/ive-had-covid-and-am-constantly-getting-colds-did-covid-harm-my-immune-system-am-i-now-at-risk-of-other-infectious-diseases-188899">I've had COVID and am constantly getting colds. Did COVID harm my immune system? Am I now at risk of other infectious diseases?</a>
</strong>
</em>
</p>
<hr>
<h2>Is there a vaccine?</h2>
<p>There are no vaccines to protect against RSV in Australia.</p>
<p>Australia’s only currently available preventative medicine is <a href="https://www.rch.org.au/rchcpg/hospital_clinical_guideline_index/Palivizumab_for_at-risk_patients/">palivizumab</a>, which is a long-acting monoclonal antibody given monthly during the RSV season. Due to its cost, it is reserved for infants at highest risk for severe RSV infection and is usually given in hospital. </p>
<p>However, several new preventative agents are in the pipeline. </p>
<p><a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-respiratory-syncytial-virus-rsv-vaccine">In May this year</a>, the US Food and Drug Administration approved the RSV vaccine Arexvy for people aged 60 and over. It is being <a href="https://www.tga.gov.au/resources/prescription-medicines-under-evaluation/arexvy-glaxosmithkline-australia-pty-ltd">considered for use</a> in Australia.</p>
<p>Results from clinical trials for RSV vaccines given to pregnant women to protect their baby for the first six months are promising. The maternal Pfizer vaccine <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2216480">has demonstrated</a> greater than 80% effectiveness against severe lower respiratory tract illness in their infants for the 90 days after birth.</p>
<p>However, safety data is being closely examined, including a <a href="https://www.bmj.com/content/381/bmj.p1021">potential risk</a> of premature birth. </p>
<p>The long-acting monoclonal antibody nirsevimab, (given as a single injection at the beginning of the RSV season) has regulatory approval in Europe and the US. It is currently <a href="https://www.tga.gov.au/resources/prescription-medicines-under-evaluation/beyfortus-astrazeneca-pty-ltd">being considered</a> for Australian children.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/fdas-approval-of-the-worlds-first-vaccine-against-rsv-will-offer-a-new-tool-in-an-old-fight-4-questions-answered-205111">FDA's approval of the world's first vaccine against RSV will offer a new tool in an old fight – 4 questions answered</a>
</strong>
</em>
</p>
<hr>
<h2>How can I protect my children in the meantime?</h2>
<p>Parents can minimise the risk of RSV by using many of the measures we’ve been using during the COVID pandemic. Encourage children to cover their mouths and noses when coughing or sneezing, and regularly wash their hands.</p>
<p>Ensuring kids stay away from school, childcare or other children when sick helps prevent the spread of many viruses, including RSV.</p>
<p><a href="https://www.rch.org.au/kidsinfo/fact_sheets/Respiratory_syncytial_virus_RSV/">Viral symptoms</a> to watch out for include difficulty feeding, cough, irritability and/or rapid breathing. If parents notice these signs or are worried about their child they should seek urgent medical assessment and not delay.</p><img src="https://counter.theconversation.com/content/208855/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Jane Tuckerman is an investigator on a project grant sponsored by Industry. Her institution has received funding from Industry (GSK) for investigator led research. She does not receive any personal payments from Industry. </span></em></p><p class="fine-print"><em><span>Ashleigh Rak receives funding from NHMRC and the Victorian Government.</span></em></p><p class="fine-print"><em><span>Danielle Wurzel receives funding from NHMRC, MRFF and has received honoraria and/or consultancy fees from MSD, Sanofi, GSK which have been paid into her research fund.</span></em></p><p class="fine-print"><em><span>Margie Danchin receives funding from NHMRC, MRFF, WHO, DFAT and the Victorian Government. She is chair, Australian Regional Immunisation Alliance. </span></em></p>Even otherwise healthy children can end up in hospital with this winter respiratory virus.Jane Tuckerman, Senior Research Officer, Murdoch Children's Research InstituteAshleigh Rak, Research Nurse Coordinator, Murdoch Children's Research InstituteDanielle Wurzel, Paediatric Respiratory Physician, and Honorary Fellow Manager, Murdoch Children's Research InstituteMargie Danchin, Paediatrician at the Royal Childrens Hospital and Associate Professor and Clinician Scientist, University of Melbourne and MCRI, Murdoch Children's Research InstituteLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2085162023-07-21T13:43:42Z2023-07-21T13:43:42ZSkin, mouth, lungs … it’s not just your gut that has a microbiome<figure><img src="https://images.theconversation.com/files/537488/original/file-20230714-19-nlny8l.jpg?ixlib=rb-1.1.0&rect=0%2C6%2C4500%2C2984&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/pink-blue-viruses-bacteria-various-shapes-749203252">ImageFlow/Shutterstock</a></span></figcaption></figure><p>A lot has been written and said about the gut microbiome – the community of bacteria, viruses, fungi and <a href="https://www.britannica.com/science/archaea">archaea</a> that lives in our intestines. But the gut is not the only place that has a microbiome. The mouth, nose, skin, lungs and genitals have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290017/">microbiomes of their own</a>. And they all play an important role in our health. </p>
<p>Here is a brief introduction to each one. </p>
<h2>Oral microbiome</h2>
<p>Arguably, this was the first microbiome discovered. </p>
<p>In the late 1600s, Antonie van Leeuwenhoek, a Dutch scientist, scraped the inside of his mouth and examined the contents under a microscope. There <a href="https://www.nature.com/articles/d42859-019-00006-2">he found</a> “many very little living animalcules, very prettily a-moving”. Today, we know that there are more than just “animalcules”, as Van Leeuwenhoek called bacteria, but fungi and viruses too. </p>
<p>This collection of microbes, among other things, aids <a href="https://journals.sagepub.com/doi/pdf/10.1177/0022034515606045?casa_token=GPHITOrnYYQAAAAA:ObRJykEn6mfriF_dv2iDxNR0KD0Ian0nEVw-Txt8CcNFN6vX2QiVuyG56kn6bAKRT6eoqAQmR42nHg">digestion</a> by breaking down complex carbohydrates into simpler sugars so that the gut can more easily absorb them. </p>
<p>As with all microbiomes, the oral microbiome competes with harmful bacteria for resources and space. When the balance of microorganisms in the mouth is disrupted, it can lead to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6503789/">cavities, gum disease and infections</a>.</p>
<p>Good <a href="https://www.sciencedirect.com/science/article/pii/S019643991300041X?casa_token=59XPqoC2RXIAAAAA:Go0cyqIFg99BAsdgZCuvOfd2P5D2xLEQpHYe5SBHk5tfSgLN4R0ji1oOWpk80PcYo5oTmowhGGA">oral hygiene and a healthy diet</a> can ensure that good microbes prevail.</p>
<h2>Nasal microbiome</h2>
<p>Moving north, we find the <a href="https://microbiomejournal.biomedcentral.com/articles/10.1186/2049-2618-2-27">nasal microbiome</a>, which helps to filter and trap particles from the air we breathe. </p>
<p>While the nasal microbiome has <a href="https://www.news-medical.net/news/20220905/The-role-of-nasal-microbiome-in-Parkinsons-disease.aspx">over a hundred strains</a> of bacteria, only two to ten species make up 90% of the microbiome. </p>
<p>These bacteria have a symbiotic relationship – you scratch my back and I’ll scratch yours. However, imbalances in the nasal microbiome can occur as a result of environmental exposures (such as air pollution), genetics or problems with our immune system. These imbalances have been linked to conditions such as <a href="https://link.springer.com/article/10.1007/s11882-014-0485-x">chronic sinusitis, nasal allergies and a higher risk of respiratory infections</a>.</p>
<p>A small study from Portugal found that wine tasters have fewer nasal bacteria and less diverse bacterial species than non-wine tasters. One of the researchers, Lucía Perez-Pardal, <a href="https://www.newscientist.com/article/2368212-wine-experts-unique-nasal-microbiome-may-affect-their-smell-and-taste/">told New Scientist</a> that the alcohol molecule dehydrates bacteria. “It removes water from their membranes and they explode,” Perez-Pardal said. “If you kill the bacteria often, you don’t give enough time for repopulation.” </p>
<figure class="align-center ">
<img alt="Person smelling wine" src="https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/537848/original/file-20230717-116180-9c9k50.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">Wine tasters have fewer nasal bacteria.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/professional-sommelier-tasting-wine-382807699">Dmytro Zinkevych/Shutterstock</a></span>
</figcaption>
</figure>
<h2>Skin microbiome</h2>
<p>A complex <a href="https://www.nature.com/articles/nrmicro.2017.157%E2%80%99">community of microorganisms</a> lives on our skin’s surface and deeper layers. </p>
<p>The skin microbiome includes bacteria, fungi and viruses. These microorganisms play an important role in <a href="https://www.nature.com/articles/nrmicro2537">keeping our skin healthy</a> and protecting against harmful bacteria. </p>
<p>Imbalances in the skin microbiome have been associated with skin conditions like <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/exd.13296">acne</a>, <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/ajd.12435?casa_token=_vTQt1bYR2wAAAAA:tk1nu6_YheOO2ZYbSCloEk3Pdeq1hQ7JI1uHvEK4hlC3jYV_F1yftbaedM3ggcTcMQIs4_ht7b8sfZQ6">eczema</a>, <a href="https://www.nature.com/articles/s41522-017-0022-5">psoriasis</a> and <a href="https://link.springer.com/article/10.1007/s11882-015-0567-4">dermatitis</a>.</p>
<p>A <a href="https://www.biorxiv.org/content/10.1101/2023.01.30.526239v1">study published earlier this year</a>, which is yet to be peer-reviewed, found that two bacterial species, <em>Cutibacterium acnes</em> and <em>Staphylococcus epidermidis</em> were associated with a decline in collagen levels – the scaffolding that keeps your skin young-looking. Expect new anti-ageing treatments that target these bugs to be on the market shortly.</p>
<h2>Lung microbiome</h2>
<p>The one part of the body that was long thought to be sterile turns out to have <a href="https://www.sciencedirect.com/science/article/pii/S1931524412000679?casa_token=WYVD7Ud2GvoAAAAA:ik5-S3DTadrFC1GAtW-VcUeGWNBXHOdtDISU2EQr6Nq4dkvcpwcVraVZN5W48y3c2yrAJj8leeY">a microbiome</a> too. The lung microbiome is not as diverse as the other biomes, mainly consisting of bacteria.</p>
<p>It is believed that these bacteria come from the mouth and nose, making their way into the lungs when we inhale small amounts of oral and nasal secretions. </p>
<p>The lung microbiome plays a role in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297685/">immune responses and respiratory health</a>. Disruptions in the lung microbiome can make us more susceptible to infections and <a href="https://www.nature.com/articles/s41579-022-00821-x">respiratory diseases</a> such as asthma, chronic obstructive pulmonary disease (COPD) and pneumonia.</p>
<h2>Genital microbiome</h2>
<p>Heading further south, we have the vaginal microbiome in females and the penile microbiome in males. </p>
<p>In females, the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045142/">vaginal microbiome</a> is mainly composed of bacteria, particularly <em>Lactobacillus</em> species. This microbiome helps maintain a <a href="https://www.sciencedirect.com/science/article/pii/S1043276011000919?casa_token=WZz-BqGy9dsAAAAA:eIY0U2o2ZY_cbAb3wtccaVg-GnuS7xZjoKdtNLH_XmGHpjAUylbSBI95S751CuZYaR77ISz7Na8">healthy vagina</a> by creating an acidic environment that prevents the growth of harmful bacteria and promotes a balanced microbial community. </p>
<p>When the vaginal microbiome is out of balance, it can lead to conditions such as bacterial <a href="https://www.annualreviews.org/doi/abs/10.1146/annurev-micro-092611-150157">vaginosis and yeast infections</a>. </p>
<p>The <a href="https://www.frontiersin.org/articles/10.3389/fcimb.2020.00433/full?fbclid=IwAR1DNUUAulyCt74OueMh0-vSjG5TQJ3b68IS_9l4-wW3evgqIS2ZvUnsGZI">penile microbiome</a> in males also contributes to genital health, although it has been less extensively studied. </p>
<p>Imbalances in the penile microbiome might lead to conditions such as <a href="https://www.sciencedirect.com/science/article/pii/S0090429522001765?casa_token=lJHsEh9KWlcAAAAA:k636tJtmU3X_4oPaw3TarARm7fV1ZNRaQLizS6x6_ozgeBQHq2akVQYPpNIa56r0gEDXDUzgo0k">urinary tract infections</a>.</p>
<h2>Gut microbiome</h2>
<p>The <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4290017/">gut microbiome</a> is one of the most well-known and influential microbiomes in our bodies. It’s a vast collection of microorganisms, including bacteria, viruses, fungi and archaea. </p>
<p>The gut microbiome is essential for digestion, metabolism and developing our immune system. It helps break down complex carbohydrates, produces vitamins, including vitamin K and various B vitamins, and helps us absorb nutrients. </p>
<p>Imbalances in the gut microbiome have been linked to conditions like <a href="https://link.springer.com/article/10.1186/s40168-021-01018-9">inflammatory bowel diseases</a>, obesity, <a href="https://link.springer.com/article/10.1007/s13679-019-00352-2">type 2 diabetes</a>, and <a href="https://idp.nature.com/authorize/casa?redirect_uri=https://www.nature.com/articles/s41380-022-01479-w&casa_token=tn1Inant-p0AAAAA:8bf9UWD1Z22lHGWkLXegh-62NsgqbEiKbHRgfFjQXT_MYFbhPTGvlxg0S84lAoijkF_o5-To3rX78pV36A">mental health disorders</a>, such as depression and anxiety. </p>
<p>There are various ways to keep the gut microbiome healthy or rebalance it when it gets out of whack. These include taking probiotics (beneficial bacteria) and prebiotics (fibres that feed the bacteria). It can also be done with a <a href="https://www.theguardian.com/australia-news/2022/nov/13/a-coup-for-poo-why-the-worlds-first-faecal-transplant-approval-matters">faecal microbiota transplant</a> (transferring healthy microbiota from a donor to a recipient), also known as a poo transplant.</p>
<p><a href="https://link.springer.com/article/10.1007/s00281-020-00814-z">These biomes</a> in our bodies are not isolated entities. They interact with each other in complex ways. For example, the oral and nasal microbiomes can affect the health of our respiratory system.</p>
<p>Disruptions in the gut microbiome can influence our <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/apm.13225">immune system</a> and affect other biomes. The skin microbiome can interact with the genital microbiome and with microbes from our environment. </p>
<p>Recognising the interconnectedness of these biomes reminds us that our body is a holistic ecosystem where imbalances in one area can have consequences throughout the entire microbial landscape. Understanding these interactions <a href="https://www.nature.com/articles/nrmicro2973">opens up new avenues</a> for improving people’s health.</p><img src="https://counter.theconversation.com/content/208516/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>Most people have heard of the gut microbiome, but the lungs, skin, mouth and genitals all have their own unique microbiome.Samuel J. White, Senior Lecturer in Genetic Immunology, Nottingham Trent UniversityPhilippe B. Wilson, Professor of One Health, Nottingham Trent UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2072862023-07-12T12:38:49Z2023-07-12T12:38:49ZStrep throat can easily be confused with throat infections caused by viruses – here are a few ways to know the difference<figure><img src="https://images.theconversation.com/files/536374/original/file-20230707-23-bxbi1g.jpg?ixlib=rb-1.1.0&rect=0%2C9%2C6640%2C4220&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Strep is most common in children between the ages of 5 and 15.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/male-pediatrician-examining-little-child-patients-royalty-free-image/1306247195?phrase=doctor+checking+for+strep&adppopup=true">aquaArts studio/E+ via Getty Images</a></span></figcaption></figure><p>“My sore throats, you know, are always worse than anybody’s.”</p>
<p>So declares Mary to Anne in “<a href="https://jasna.org/austen/works/persuasion/">Persuasion</a>,” Jane Austen’s 1817 book. Most of us can relate to this feeling. There is no such thing as “just a sore throat.” The pain, headache, fever and aches associated with a sore throat can make you feel terrible.</p>
<p>While sore throats can occur at any time of year, strep throat is <a href="https://www.cdc.gov/groupastrep/surveillance.html#">more common in the fall, winter and early spring</a>.</p>
<p>I am a <a href="https://facultyprofiles.tufts.edu/allen-shaughnessy">professor of family medicine</a>, a pharmacist and an expert on evidence-based medicine. My work involves the evaluation of research performed by others, and I have been following and analyzing research findings on strep for the past 30 years. </p>
<p>Many people incorrectly assume that all sore throats are due to strep throat, a bacterial infection of the pharynx, the middle throat area behind the nose and mouth, and patients often come to our family medicine office wanting to be checked and treated for strep with antibiotics.</p>
<p>However, neither testing nor treatment is always needed for a sore throat. Regardless of the cause, rest and pain relievers form the cornerstone of sore throat treatment.</p>
<p>Here’s some guidance on whether and when testing is necessary.</p>
<h2>Bacterial versus viral sore throats</h2>
<p>Most <a href="https://www.cdc.gov/antibiotic-use/sore-throat.html">sudden-onset sore throats</a> are caused by viruses – the same ones that cause the common cold, the seasonal flu and COVID-19. There are <a href="https://www.nih.gov/news-events/nih-research-matters/understanding-common-cold-virus#">more than 200 viruses</a> that can cause sore throat and other symptoms related to the common cold. </p>
<p>But bacteria can also be the culprits behind a sore throat. One of the most common examples is <a href="https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html#">strep throat</a>, or <a href="https://www.cdc.gov/streplab/groupa-strep/index.html">group A pharyngitis</a>.</p>
<p>Strep is caused by certain strains of <em>Streptococcus pyogenes</em> bacteria.
There are many species of strep; other common forms of strep that cause different infections in humans include “<a href="https://www.cdc.gov/groupbstrep/index.html">group B strep</a>” and “<a href="https://www.icliniq.com/articles/infectious-diseases/group-d-streptococcus-infections">group D strep</a>.” Group A strep usually lives peacefully among the many other types of bacteria growing on our skin and doesn’t cause any problems, until we get a break in the skin such as a cut or a scrape. This allows it to overwhelm the immune system’s ability to keep it in check.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A teenage girl is lying on a sofa, feeling unwell and holding a thermometer in her mouth to check her temperature." src="https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/536145/original/file-20230706-18-5qdns0.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>
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<span class="caption">Fever, headache and confusion can be symptoms of a severe case of strep.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/sick-teenager-resting-at-home-and-monitoring-royalty-free-image/1482421648?phrase=strep+throat&adppopup=true">RealPeopleGroup/E+ via Getty Images</a></span>
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<p>Group A strep can also live in the back of the throat – up to 30% of people without any evidence of a sore throat will have <a href="https://doi.org/10.3389/fcimb.2019.00137">this strain in their throat</a>. <a href="https://www.cdc.gov/groupastrep/diseases-public/strep-throat.html#">Up to 3 in 10 children and 1 in 10 adults</a> feeling sick with a sore throat due to a virus or other cause will test <a href="https://doi.org/10.1371/journal.pntd.0006335">positive for group A strep</a>. That means that people with a sore throat caused by a virus could also be positive for strep, even if it’s not causing the symptoms.</p>
<p>Not all group A strep bacteria are the same, though. Some varieties are better at evading the immune system than others and can grow quickly. Others produce byproducts that can cause a sore throat and sometimes lead to <a href="https://www.mayoclinic.org/diseases-conditions/tonsillitis/symptoms-causes/syc-20378479">tonsillitis</a>, an infection of the tonsils, or cause ear or <a href="https://www.cdc.gov/antibiotic-use/sinus-infection.html">sinus infections</a>. </p>
<p>Still other strep strains produce a toxin that can cause a characteristic <a href="https://www.cdc.gov/groupastrep/diseases-public/scarlet-fever.html">skin rash</a> or lead to effects on the <a href="https://www.cdc.gov/groupastrep/diseases-public/rheumatic-fever.html">heart</a>, <a href="https://www.cdc.gov/groupastrep/diseases-public/post-streptococcal.html">kidneys</a> or even the <a href="https://www.nimh.nih.gov/health/publications/pandas">brain</a>. </p>
<p>Rarer still, group A strep can enter the bloodstream and cause <a href="https://www.mayoclinic.org/diseases-conditions/toxic-shock-syndrome/symptoms-causes/syc-20355384">toxic shock syndrome</a>, a life-threatening, overwhelming infection. These latter conditions are examples of invasive strep, meaning that the infection is in parts of the body typically free from germs; they <a href="https://www.cdc.gov/groupastrep/igas-infections-investigation.html">seem to be on the rise</a> after a marked <a href="https://www.cdc.gov/groupastrep/igas-infections-investigation.html">reduction in their occurrence during the COVID-19 pandemic</a>. </p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/W50S0dCCFPs?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Like other illnesses that made a comeback after COVID-19 prevention measures were relaxed, strep cases have returned to pre-pandemic levels.</span></figcaption>
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<h2>To test or not to test</h2>
<p>Doctors or other clinicians can easily test for strep by using a swab to collect a bit of the fluid from the back of the throat. This sample can identify group A strep in about a minute. </p>
<p>While researchers have been studying group A strep <a href="https://www.ncbi.nlm.nih.gov/books/NBK333430/">for over 75 years</a> and there are thousands of research papers focused on infections caused by strep, there is still <a href="https://www.nice.org.uk/guidance/ng84/chapter/Summary-of-the-evidence">controversy</a> over whether it needs to be tested for and treated. </p>
<p>To decide whether to test for group A strep, clinicians use a set of criteria based on <a href="https://www.mdcalc.com/calc/104/centor-score-modified-mcisaac-strep-pharyngitis">five questions</a> that can help determine whether strep testing is needed. These are:</p>
<p>– How old is the patient? Strep throat is most common in children <a href="https://www.cdc.gov/groupastrep/diseases-public/strep-throat.html#">between ages 5 and 15</a> and least common in <a href="https://www.cdc.gov/groupastrep/diseases-hcp/strep-throat.html#">adults over age 45</a>. </p>
<p>– Are the tonsils swollen or do they have a white or yellow coating? Both conditions often accompany strep. However, this question alone isn’t definitive, since viruses can also affect the tonsils.</p>
<p>– Are the <a href="https://www.verywellhealth.com/cervical-lymph-nodes-2252142">cervical lymph nodes</a> swollen or tender? Normally these bumps, which are in the front of the neck along the sides of the windpipe, cannot be seen or felt, but are often palpable when strep is present.</p>
<p>– Does the person have a fever? Lack of a fever makes strep less likely.</p>
<p>– Does the person have a cough? A cough is indicative of a viral cause and makes strep the less likely cause of the sore throat.</p>
<p>While none of these questions alone can provide a clear answer, taken together they can tell your clinician whether strep is more or less likely. </p>
<p>Using this scoring tool, an adult with a sore throat but without changes to the tonsils or lymph nodes, without a fever and with a cough has only a <a href="https://www.mdcalc.com/calc/104/centor-score-modified-mcisaac-strep-pharyngitis">1 in 40 chance, or 2.5%, of having strep throat</a>. For such patients, a strep test is not necessary. </p>
<p>On the other hand, when a first grader meets all five of these criteria, there is a 50% chance that strep is causing his or her sore throat. Based on recent research I have reviewed, by using these questions <a href="https://doi.org/10.7326/0003-4819-159-9-201311050-00003">adults can determine</a> when strep is the likely cause of a sore throat. </p>
<p>In the <a href="https://www.nice.org.uk/guidance/ng84">United Kingdom</a> and <a href="https://doi.org/10.1370/afm.741">other European countries</a>, doctors do not routinely test for strep. Antibiotic treatment can at times <a href="https://www.cdc.gov/antibiotic-use/community/pdfs/aaw/au_arent_always_the_answer_fs_508.pdf">cause allergic reactions, rash, diarrhea, stomach upset, yeast infections and other side effects</a>. Authorities in these countries feel any benefit of testing and treatment does not outweigh these risks.</p>
<h2>Treatments for strep</h2>
<p>Once group A strep is confirmed, doctors may prescribe an antibiotic treatment. </p>
<p>Penicillin or amoxicillin are the most commonly prescribed antibiotics for strep. These medicines will not reduce pain or tiredness but may help symptoms resolve earlier, typically by <a href="https://www.nice.org.uk/guidance/ng84/chapter/Summary-of-the-evidence">about a day</a>. Doctors may also suggest use of a pain reliever such as acetaminophen or ibuprofen to help relieve symptoms.</p>
<p>Antibiotic treatment does not seem to lower the likelihood of <a href="https://doi.org/10.1136/bmj.38503.706887.AE1">spread of the infection between children</a> – which is common in schools and dormitories – <a href="https://doi.org/10.1136/bmj.f6867">or adults</a>.</p>
<p>Health care practitioners recommend staying home until fever has subsided. They also recommend taking the full course of antibiotics, even if the symptoms have abated. </p>
<p>With sore throats causes by viruses – against which antibiotics are ineffective – few treatments exist aside from using pain relievers to help soothe immediate symptoms. For this reason and because <a href="https://www.cdc.gov/antibiotic-use/index.html">antibiotic overuse is a major problem in the U.S.</a>, it is best not to assume that your sore throat is caused by strep and to treat it accordingly.</p><img src="https://counter.theconversation.com/content/207286/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Allen Shaughnessy 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>Despite an abundance of research on strep, there is still a great deal of debate in the scientific community over whether and when people should get tested and treated for it.Allen Shaughnessy, Professor of Family Medicine, Tufts UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2081562023-06-23T13:39:47Z2023-06-23T13:39:47ZDirty tea towels are breeding grounds for harmful bacteria – here’s how to clean them properly<figure><img src="https://images.theconversation.com/files/533147/original/file-20230621-15-81vklh.jpg?ixlib=rb-1.1.0&rect=123%2C0%2C6227%2C4218&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Yep, when you've finished, both of those need to go in the wash.</span> <span class="attribution"><a class="source" href="https://www.pexels.com/photo/close-up-of-women-in-pattern-dresses-drying-cutlery-with-tea-towels-6956744/">pexels/karolina grabowska</a></span></figcaption></figure><p><a href="https://link.springer.com/article/10.1023/A:1016378226861">Kitchens</a> can harbour all sorts of germs and bacteria. These can arrive via humans, pets, uncooked food or even plants, meaning that a high proportion of <a href="https://academic.oup.com/jambio/article-abstract/119/2/582/6717307?redirectedFrom=fulltext">foodborne infections</a> are acquired directly within the home. </p>
<p>An important cleaning aid in most kitchens is the tea towel, also known as a dishcloth. Usually made of cotton or linen, they are used to dry wet hands and kitchen implements as well as wiping down surfaces – so play an important role in kitchen hygiene. </p>
<p>But, because hands and uncooked fresh produce are often rich in a diverse variety of germs, tea towels are prone to picking up the bacteria they come into contact with. </p>
<p>Indeed, in a <a href="https://www.semanticscholar.org/paper/Achieving-hygiene-in-the-domestic-kitchen%3A-the-of-Cogan-Slader/ffc798f7219afc6f986d6f18c62e6e496e7e0161">study</a> that used tea towels to wipe down chopping boards that had been used to prepare raw chicken with salmonella (which can cause diarrhoea, fever and stomach cramps), 90% of the cloths became contaminated with salmonella, too.</p>
<p><a href="https://www.tandfonline.com/doi/abs/10.1080/09603129509356839?src=recsys">Several studies</a> have looked at the germs tea towels typically carry in domestic kitchens. One study sampled 100 used tea towels and found a marked presence of <a href="https://www.tandfonline.com/doi/abs/10.1080/09603120050127202?src=recsys">staphylococcus aureus</a> <em>Staphylococcus aureus</em>, which is often found on the skin but is also a pathogen that can cause a variety of issues such as abscesses, joint infections and even pneumonia.</p>
<figure class="align- centre ">
<img alt="Tea towels hanging to dry on the oven door." src="https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=382&fit=crop&dpr=1 600w, https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=382&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=382&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=480&fit=crop&dpr=1 754w, https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=480&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/533151/original/file-20230621-15-620nos.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=480&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Dirty tea towels are a breeding ground for bacteria and foodborne illnesses.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/closeup-teatowels-on-rack-2293555605"> Joe Kuis/Shutterstock</a></span>
</figcaption>
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<p>Tea towels are good at picking up germs which is important as another <a href="https://www.tandfonline.com/doi/abs/10.1080/09603129509356839?src=recsys">study of 46 kitchens</a> found a wide range of harmful bacterial species living on kitchen surfaces, which are often cleaned by tea towels. </p>
<p>Surfaces were found to have <em>Enterobacter</em> (which can cause respiratory tract infections, skin infections, urinary tract infections and heart, bone and eye infections), <em>Klebsiella</em> (which has been linked to serious infections of the lungs, bladder, brain and blood), and <em>E. coli</em> (which can cause upset stomachs and urinary tract infections). </p>
<p>Several kitchens also had <em>Pseudomonas aeruginosa</em>, which can cause lung infections. <em>Bacillus subtilis</em>, which can lead to eye infections and abscesses, was also found in more than half of the kitchens sampled. And all of the samples from the kitchens were found to have <em>Staphylococcus</em> and <em>Micrococcus</em>. In people with weak immune systems, <em>Micrococcus</em> has been linked to lung infections, such as pneumonia and septic arthritis along with eye and heart infections.</p>
<p>The levels and types of germs found on these tea towels were influenced by how they were used, how often they were washed and how long they were dried for. <a href="https://www.sciencedirect.com/science/article/pii/S0956713522003887?via%3Dihub">Rinsing tea towels in hot water</a> at 60°C was found to reduce levels of bacteria later spread by contaminated cloths, which is important as infection likelihood is often related to how many bacteria you ingest.</p>
<h2>Clean your cloths</h2>
<p>These studies suggest there is an infection risk from tea towels and that most kitchen cloths may be contaminated with high levels of bacteria. It’s easy, then, for these germs to transfer on to food preparation surfaces, potentially causing serious food poisoning. </p>
<p>The infection risk of using tea towels is well-recognised by the medical profession. Indeed, in UK hospitals, fabric <a href="https://www.leicspart.nhs.uk/wp-content/uploads/2021/02/Food-Hygiene-for-Ward-and-Therapy-kitchens-Infection-Prevention-Policy-exp-Feb-24.pdf">tea towels are not allowed</a>. Instead, patient crockery, cutlery and food preparation work surfaces are cleaned and dried with disposable paper towels. </p>
<p>One of the reasons tea towels act as such good microbial reservoirs is that they are often damp as they are used to absorb moisture and mop up spills. <a href="https://www.sciencedirect.com/science/article/pii/S0956713522003887?via%3Dihub">Water enables germs to grow</a>. And so a moist tea towel left in a warm kitchen provides an ideal environment for bacteria to multiply. This is particularly the case if food traces are present, too. </p>
<p>So what’s the best way to sanitise your used tea towel? Tea towels that are hung up in the air tend to dry faster than cloths stored and squeezed into balls, which can affect levels of bacteria in the towels. </p>
<p><a href="https://www.sciencedirect.com/science/article/pii/S0956713522003887?via%3Dihub">Laboratory experiments</a> that involved covering tea towels in salmonella, found that the bacteria multiplied in all types of cloths that were crumpled. But levels of bacteria were reduced by 1,000 times if the tea towels were hung to dry for 24 hours at room temperature. </p>
<h2>Reduce the germs</h2>
<p>To avoid tea towels spreading germs around the kitchen, it’s recommended that the cloths are washed regularly and when they get wet, are allowed to dry completely before being used again. Using <a href="https://www.food.gov.uk/sites/default/files/media/document/cloths.pdf">disposable cloths</a> or paper towels for heavily contaminated areas, such as those involving raw meat, could also help to stop the spread of bacteria. </p>
<p>In terms of tea towel hygiene, you should clean and thoroughly dry your kitchen towel <a href="https://www.food.gov.uk/sites/default/files/media/document/cloths.pdf">at least once a day</a> or after each use. The UK government recommends that tea towels should be sanitised by washing them in a washing machine with laundry detergent on a hot wash cycle of 90°C. </p>
<figure class="align-center ">
<img alt="Tea towels drying on a clothesline." src="https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/533152/original/file-20230621-18-piu85o.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">
<figcaption>
<span class="caption">Daily washing of tea towels is crucial for kitchen hygiene.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/colourful-towels-tea-hung-outside-dry-1655802655"> Tony Skerl/Shutterstock</a></span>
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<p>Laundry detergents contain hard water softeners, surfactants (which increase the wetting effect of water by reducing its surface tension), detergents, bleaches and digestive enzymes. Food stains on tea towels will probably be a mixture of proteins, fats and carbohydrates, which the enzymes degrade. </p>
<p>And the detergent helps to dissolve the stains, which are released into the washing water. Since proteins and fats are also involved in the attachment of bacteria to surfaces, laundry detergents will help to detach and so reduce bacteria levels in tea towels. </p>
<p>If you <a href="https://www.food.gov.uk/sites/default/files/media/document/cloths.pdf">wash tea towels</a> by hand, ensure any obvious food and dirt are removed by rinsing in hot water with detergent before disinfection. After washing, you can sanitise any microbes remaining using boiling water or a disinfectant such as bleach, diluted as per the manufacturer’s instructions. </p>
<p>Ironing tea towels on a hot setting will also effectively sanitise as the temperature is <a href="https://www.food.gov.uk/sites/default/files/media/document/cloths.pdf">above 90°C</a>.
You should also store your laundered tea towels in a dry, clean area, away from any uncooked food and grubby hands.</p><img src="https://counter.theconversation.com/content/208156/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Primrose Freestone 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>A microbiologist on the deadly germs lurking in your kitchen and why you need to wash tea towels and dishcloths more often.Primrose Freestone, Senior Lecturer in Clinical Microbiology, University of LeicesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2050692023-06-05T14:25:30Z2023-06-05T14:25:30ZHepatitis B is a life-threatening liver infection – our machine learning tool could help with early detection<figure><img src="https://images.theconversation.com/files/529046/original/file-20230530-15-9wf3s7.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">Getty Images</span></span></figcaption></figure><p>More than <a href="https://www.who.int/news-room/fact-sheets/detail/hepatitis-b">296 million people</a> worldwide live with hepatitis B, a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). Most don’t know they are infected, so they don’t get medical care. Clinical care improves the patient’s outcome and can prevent them from infecting others. </p>
<p>Early detection of HBV-infected patients could therefore improve patient prognosis and stop transmission within populations. </p>
<p>The recommended test for HBV is an <a href="https://apps.who.int/iris/bitstream/handle/10665/254621/9789241549981-eng.pdf">enzyme immunoassay</a>. It detects the hepatitis B surface <a href="https://www.britannica.com/science/antigen">antigen</a> – a substance that is a sign of the presence of the virus in the person’s body. </p>
<p>But these chemical tests are very <a href="https://apps.who.int/iris/bitstream/handle/10665/254621/9789241549981-eng.pdf">expensive</a> and need dedicated facilities. They are generally out of reach for people in low-resource settings, where laboratories are few and isolated. Clinicians in these settings work with limited resources against <a href="https://www.afro.who.int/news/91-million-africans-infected-hepatitis-b-or-c">a silent killer</a> that may not show obvious symptoms for decades until the liver is severely damaged. </p>
<p>Part of the solution for public health challenges like this may lie in <a href="https://theconversation.com/what-machine-learning-can-offer-nigerias-healthcare-system-163593">machine learning</a>. This refers to the ability of computers to make sense of large amounts of information – and to build on their own “knowledge”.</p>
<p>We are among a group of researchers at the <a href="https://nceph.anu.edu.au/">Australian National University</a> who study machine learning and infectious disease. Our <a href="https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-021-06800-6">earlier research</a> found that the prevalence of HBV in Nigeria was high (9.5%, where anything above 8% is considered high). And the levels of infection varied significantly across geopolitical zones. </p>
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Read more:
<a href="https://theconversation.com/hepatitis-b-in-nigeria-fresh-data-to-inform-prevention-and-care-173018">Hepatitis B in Nigeria: fresh data to inform prevention and care</a>
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<p>Access to affordable testing was a problem in the country. So we <a href="https://www.nature.com/articles/s41598-023-30440-2">developed a tool</a> to help clinicians detect hepatitis B infections earlier.</p>
<p>Using Nigerian patient data, we developed an algorithm that learns from the patient data, identifies patterns, and makes intelligent decisions to provide alerts and detection of a patient’s HBV infection status. The aim is to enhance clinical decision-making and improve patient outcomes. Enabling earlier care should give millions of people a better quality of life and help reduce HBV prevalence.</p>
<h2>How did we do the work?</h2>
<p>To build this tool, we worked closely with colleagues at the <a href="https://nimr.gov.ng/">Nigerian Institute of Medical Research</a>. They provided access to data from 916 anonymous patients, in an ethically approved manner. The institute is Nigeria’s foremost medical research institute and it hosts a dedicated hepatitis B clinic.</p>
<p>We used the results of normal blood tests that measure red and white blood cells, salts, enzymes and other blood chemicals, along with results of tests for hepatitis B. Routine blood tests can be very useful in facilitating early diagnosis if the subtle interactions between measurements can be spotted. Patterns of interactions may be a signal of disease. But it’s easy to miss them. </p>
<p>Using the data, we trained an algorithm to identify pathology markers that predict a patient’s HBV infection status. One reason machine learning is so powerful is that it does not require humans to tell the computer which features to identify. Our algorithm sifts through the data to find patterns that are common to patients with HBV infection and then match those patterns in people it has not seen before. </p>
<p>Once validated, the algorithm can be integrated into routine clinical workflow in a real-world clinical setting, as an intelligent decision support system. This will help detect HBV infections earlier, without resorting to expensive immunoassay. </p>
<h2>What did we find?</h2>
<p>For the 916 people in <a href="https://www.nature.com/articles/s41598-023-30440-2">our study</a>, our algorithm could reliably make an intelligent call to accurately predict those infected with HBV. Its discrimination threshold was 90% — indicating that the algorithm was highly accurate.</p>
<p>We then translated this into a user-friendly, web-accessible app to use in further studies. The decision support tool, <a href="https://hepblivetest.app/">Hep B LiveTest</a>, was designed as a prototype.</p>
<p>The tool found that a combination of two enzymes, patient age and white blood cell count was the strongest predictor of HBV infection. The two enzymes are aspartate aminotransferase and alanine aminotransferase. When levels of these in the blood are high, it may indicate potential liver damage. Serum albumin, a liver function marker, was also identified as an important predictive marker of infection.</p>
<p>A <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.23609">study of Chinese patients</a> showed trends similar to those suggested by our algorithm. Alanine aminotransferase and serum albumin were the most prominent predictors.</p>
<h2>What’s next?</h2>
<p>It is important to recognise the limitations of machine learning. Before a tool like this is put to work in routine clinical practice, it needs to be validated using diverse data. </p>
<p>Our machine learning tool was trained with data from Nigeria, so its performance may be limited to that setting. We are in the process of training our algorithm with more data from other sources and validating its robustness in other settings. This will inform how broadly applicable our algorithm is and how well it might work in other populations – particularly in settings with a low prevalence of hepatitis B infections.</p>
<p>Though our machine learning tool is only a first test, the results are highly encouraging. <a href="https://news.un.org/en/story/2021/07/1096592">A person dies from viral hepatitis B every 30 seconds</a>. We hope to put our system to work soon in the urgent fight against this <a href="https://www.nature.com/articles/d44148-022-00128-2">vaccine-preventable disease</a>. </p>
<p>We believe that machine learning has a role in enhancing the World Health Organization’s targets of <a href="https://apps.who.int/iris/bitstream/handle/10665/246177/WHO-HIV-2016.06-eng.pdf?sequence=1&isAllowed=y">eliminating viral hepatitis as a public health problem by 2030</a>.</p><img src="https://counter.theconversation.com/content/205069/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Brett A. Lidbury receives funding from the Quality Use of Pathology Program (QUPP) - Commonwealth Department of Health. He holds a Fellowship with the Royal College of Pathologists of Australasia (RCPA) Faculty of Science, and collaborates with the RCPA Quality Assurance Programme (RCPAQAP). </span></em></p><p class="fine-print"><em><span>Busayo I. Ajuwon 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>Machine learning can spot patterns in patient data and help detect hepatitis B earlier, which could save lives.Busayo I. Ajuwon, Research Scientist, Australian National UniversityBrett A. Lidbury, Associate ProfessorLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2029322023-05-31T12:38:14Z2023-05-31T12:38:14ZCytomegalovirus lies dormant in most US adults and is the leading infectious cause of birth defects, but few have heard of it<figure><img src="https://images.theconversation.com/files/529162/original/file-20230530-19-du6gsi.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C2121%2C1412&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Cytomegalovirus belongs to the same virus family, _Herpesviridae_, as cold sores and chickenpox.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/electron-microscope-image-of-cytomegalovirus-royalty-free-image/1134489724">Callista Images/Image Source via Getty Images</a></span></figcaption></figure><p>“Why didn’t anyone tell me about this virus?” is a frequent response I hear from parents upon learning their newborn is infected with <a href="https://www.nationalcmv.org/">cytomegalovirus, or CMV</a>. Although <a href="https://doi.org/10.1186/s12889-022-13971-7">more than half of the U.S. population</a> will be infected with CMV by the age of 40 and the disease is <a href="https://doi.org/10.1002/rmv.2034">common worldwide</a>, few people have ever heard of it.</p>
<p>CMV belongs to the <a href="https://www.merckmanuals.com/home/infections/herpesvirus-infections/overview-of-herpesvirus-infections">same virus family</a> as cold sores and <a href="https://theconversation.com/the-chickenpox-virus-has-a-fascinating-evolutionary-history-that-continues-to-affect-peoples-health-today-168636">chickenpox</a> and, like those viruses, <a href="https://theconversation.com/chickenpox-and-shingles-virus-lying-dormant-in-your-neurons-can-reactivate-and-increase-your-risk-of-stroke-new-research-identified-a-potential-culprit-194627">lives in the body for life</a>. Most children and adults experience <a href="https://www.merckmanuals.com/home/infections/herpesvirus-infections/cytomegalovirus-cmv-infection">very mild or even no symptoms</a> with their initial infection. A healthy immune system is typically able to keep CMV under control so people don’t become sick or even know the virus is living in their body.</p>
<p>So if most people are unlikely to get sick from CMV at any age, then why is the virus so important to understand? As an <a href="https://www.researchgate.net/profile/Laura-Gibson-7">infectious disease and immunology specialist</a>, I have focused on this question for most of my two-decade career. One major reason is that CMV – unlike the other viruses in its family – can <a href="https://www.cdc.gov/cmv/index.html">pass from mother to fetus</a> during pregnancy. </p>
<p>Congenital CMV, or cCMV, is the most common infection before birth and the <a href="https://www.marchofdimes.org/find-support/topics/planning-baby/cytomegalovirus-and-pregnancy">leading infectious cause of birth defects</a>. About <a href="https://www.cdc.gov/cmv/congenital-infection.html">one in every 200 infants</a> – typically 20,000 to 30,000 infants in the U.S. – are born with cCMV per year, and <a href="https://doi.org/10.1016/j.jcv.2009.09.002">nearly 20%</a> of them have permanent neurodevelopmental disabilities such as hearing loss or cerebral palsy. Every year, more children are <a href="https://doi.org/10.1186/1471-2458-5-70">affected by cCMV</a> than several familiar childhood conditions like Down syndrome and fetal alcohol syndrome. Compared to later stages of pregnancy, CMV infection in the <a href="https://doi.org/10.1016/j.ajog.2020.05.038">first trimester carries the highest risk</a> of stillbirth or severe effects when the immune system and organs like the brain are developing. </p>
<p>Rates of cCMV differ significantly by race, ethnicity and other demographic factors, with Black and multiracial infants <a href="https://doi.org/10.1016/j.jpeds.2018.04.043">twice as likely</a> to have cCMV compared to other groups. Black and Native American infants also have a <a href="https://doi.org/10.1371/journal.pntd.0001140">higher risk of death</a> from cCMV compared to white infants. </p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/FTw6vE-xSwY?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Herpesviruses share the ability to stay latent in the body for life.</span></figcaption>
</figure>
<h2>Looking for CMV during pregnancy</h2>
<p>Screening for rubella, HIV and syphilis is <a href="https://www.cdc.gov/nchhstp/pregnancy/screening/index.html#">routine for early prenatal care</a> in the U.S. Counseling to avoid kitty litter to <a href="https://theconversation.com/toxoplasma-cat-poo-parasite-infects-billions-so-why-is-it-so-hard-to-study-120688">prevent toxoplasmosis</a> is also common. If CMV can infect a fetus and cause birth defects, then why aren’t pregnant people tested and treated for this virus too? </p>
<p>Prenatal CMV screening is not standard of care <a href="https://doi.org/10.1016/s1473-3099(17)30143-3">due to several limitations</a> of the current testing approach. Some available tests can be <a href="https://doi.org/10.1016/j.jcv.2012.09.015">difficult for health care providers to interpret</a>. Testing provides information about whether the parent has CMV, but it does not sufficiently predict the risk of fetal transmission or severe symptoms. </p>
<p>Prenatal screening for a healthy person with a normal pregnancy does not usually offer useful information. That’s because <a href="https://doi.org/10.1128/jvi.02392-16">anyone can have a baby with cCMV</a> regardless of whether <a href="https://doi.org/10.1093/infdis/jiy321">they tested positive or negative for it</a> before or earlier in pregnancy. CMV testing may be useful for pregnant people who are experiencing acute illness, such as prolonged fever and fatigue, or who have an abnormal fetal ultrasound.</p>
<p>Even if more accurate tests were available, there are currently no medical interventions approved by the Food and Drug Administration to reduce the risk of fetal CMV infection. <a href="https://doi.org/10.1002/uog.23596">Biweekly antibodies against CMV</a> seem to reduce fetal transmission when given around conception or during the first trimester, but CMV is rarely diagnosed that early in pregnancy.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Pregnant person touching belly" src="https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/529171/original/file-20230530-21-eyj9a0.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">Most available drugs to treat CMV are unsafe to take during pregnancy.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/pregnant-woman-touching-her-belly-royalty-free-image/1390901979">FG Trade/E+ via Getty Images</a></span>
</figcaption>
</figure>
<p>Researchers are currently evaluating the drug valacyclovir as a potential treatment to prevent fetal transmission. Valacyclovir is commonly used to prevent or treat <a href="https://www.cdc.gov/stiapp/herpes-genital_ado_adult.html">genital herpes</a> during pregnancy. Findings from a recent clinical trial in Israel suggest that valacyclovir <a href="https://doi.org/10.1016/s0140-6736(20)31868-7">may reduce the risk</a> of CMV transmission to the fetus.</p>
<p>In general, valacyclovir does not work as well as <a href="https://www.drugs.com/pregnancy/ganciclovir.html">other CMV drugs</a> that people cannot take during pregnancy. As a result, a <a href="https://doi.org/10.1016/s0140-6736(20)31868-7">much higher dose is required</a> to reduce the risk of fetal CMV infection, which may cause significant side effects for pregnant people. </p>
<p>Although the use of valacyclovir to prevent cCMV is not standard in the U.S., and research on its effectiveness <a href="https://doi.org/10.1016/j.cmi.2020.04.006">remains limited</a>, the drug is used for this purpose <a href="https://doi.org/10.1016/j.jcv.2020.104351">in some areas</a> <a href="https://doi.org/10.1016/j.ajog.2016.04.003">of the world</a>.</p>
<h2>Screening newborns for CMV</h2>
<p>Like pregnant people, babies are <a href="https://www.hrsa.gov/advisory-committees/heritable-disorders/rusp">screened for many potentially serious conditions</a>. An accurate <a href="https://doi.org/10.1056/nejmoa1006561">CMV test for newborns</a> is available, and many studies <a href="https://doi.org/10.1002/rmv.1790">support the benefit</a> of <a href="https://doi.org/10.1038/s41372-019-0501-z">early CMV diagnosis</a>. So why isn’t there universal CMV screening for infants?</p>
<p>While some birth centers <a href="https://www.nationalcmv.org/overview/newborn-screening">provide early CMV testing</a>, most U.S. states <a href="https://www.nationalcmv.org/about-us/advocacy">do not mandate newborn CMV screening</a>. My team and I surveyed 33 hospitals in Massachusetts from late 2020 to early 2021 and found that <a href="https://doi.org/10.3390/ijns8040065">less than half</a> are consistently screening infants for cCMV infection. Of those, only a few have a written testing protocol. Only two hospitals performed cCMV screening on all infants admitted to the newborn nursery.</p>
<p>Standardizing public health education and CMV screening guidelines could help reduce the incidence and burden of cCMV disease on children and their families. In July 2013, <a href="https://le.utah.gov/%7E2013/bills/static/hb0081.html">Utah became the first state</a> to pass legislation mandating a CMV public education program and testing for infants who do not pass the newborn hearing screen. In February 2022, <a href="https://www.revisor.mn.gov/statutes/cite/144.064">Minnesota became the first</a> – and remains the only – state to require CMV screening of all newborns, although <a href="https://malegislature.gov/Bills/192/SD1810">Massachusetts</a> and <a href="https://iga.in.gov/legislative/2021/bills/house/1362#document-aa892856">Indiana</a> have pending universal screening bills. So far, 17 states have enacted laws requiring cCMV education or targeted screening of newborns who meet certain criteria, and many others are considering similar options.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Person holding baby closely" src="https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/529163/original/file-20230530-17-eip1bt.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">Negative health effects from cCMV may not show for a newborn until later.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/side-view-of-new-mother-comforting-her-newborn-royalty-free-image/1367022758">Juanma Hache/Moment via Getty Images</a></span>
</figcaption>
</figure>
<p>On the other hand, designing, funding and implementing a new infant screening program is <a href="https://www.hrsa.gov/advisory-committees/heritable-disorders/rusp">complex and time-consuming</a>, and may potentially divert resources from other equally important health initiatives. Most newborns with cCMV appear physically normal at birth and <a href="https://www.cdc.gov/cmv/congenital-infection.html">develop normally over their lifetime</a>, leading some to question the benefits of CMV screening for those children. </p>
<p>However, infants may have abnormalities that are <a href="https://doi.org/10.1038/s41372-019-0501-z">not visible at birth</a>, and there isn’t a reliable way to predict whether they will have progressive health problems. Without screening all newborns for CMV, those who appear normal at birth will not be fully evaluated, considered for treatment or monitored for effects that develop later, such as hearing loss.</p>
<h2>Spreading CMV awareness, not infection</h2>
<p>Decreasing the incidence of cCMV infection is unlikely without increasing awareness. Most people <a href="https://doi.org/10.1089/jwh.2007.0523">have not heard of CMV</a> or are <a href="https://doi.org/10.1016/j.ypmed.2012.03.009">unwaware of what they can do</a> to reduce their chances of getting CMV during pregnancy. </p>
<p>Many adults are repeatedly exposed to one of the major risk factors for CMV infection: a young child who <a href="https://doi.org/10.1016/s0022-3476(88)80314-7">regularly attends</a> <a href="https://doi.org/10.1056/nejm198911093211903">large-group child care</a>. Infections like CMV spread easily among children in settings where group play, meals and diaper changes become daily opportunities for transmission. Children can appear quite healthy but carry CMV in their saliva and urine for weeks or even months after infection. When an <a href="https://doi.org/10.1542/peds.2005-1142">unsuspecting</a> <a href="https://doi.org/10.1056/nejm198605293142204">pregnant</a> <a href="https://doi.org/10.1097/00006454-199108000-00008">caretaker</a> comes into contact with those body fluids, they can become infected as well. </p>
<p>For people who are pregnant, <a href="https://doi.org/10.1097/00006454-199603000-00013">simple behavior changes</a> such as kissing a child on the head instead of the lips, not sharing food or utensils, and frequent handwashing can significantly reduce the risk of getting CMV.</p>
<p>Educating the public, policymakers and health care providers will improve the diagnosis, prevention and treatment of cCMV, so no parent suffers the thought “If I had only known…”</p><img src="https://counter.theconversation.com/content/202932/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Laura Gibson is a member of the Scientific Advisory Board for the CMV Program at Moderna Therapeutics, Inc. She also receives research funding from Moderna. She is affiliated with the Massachusetts Congenital CMV Coalition.</span></em></p>Although testing for CMV during pregnancy isn’t routine and there isn’t universal screening for infants, there are steps pregnant people can take to protect themselves and their newborns.Laura Gibson, Associate Professor of Medicine and of Pediatrics, UMass Chan Medical SchoolLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2051452023-05-09T15:02:05Z2023-05-09T15:02:05ZRSV: we finally have a vaccine for this deadly virus<p>The first vaccine against respiratory syncytial virus (RSV) has been <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-respiratory-syncytial-virus-rsv-vaccine">approved</a> by the US Food and Drug Administration. The vaccine, named Arexvy, will be given to people 60 years and older. </p>
<hr>
<iframe id="noa-web-audio-player" style="border: none" src="https://embed-player.newsoveraudio.com/v4?key=x84olp&id=https://theconversation.com/rsv-we-finally-have-a-vaccine-for-this-deadly-virus-205145&bgColor=F5F5F5&color=D8352A&playColor=D8352A" width="100%" height="110px"></iframe>
<p><em>You can listen to more articles from The Conversation, narrated by Noa, <a href="https://theconversation.com/us/topics/audio-narrated-99682">here</a>.</em></p>
<hr>
<p>The European Medicines Agency is <a href="https://www.bmj.com/content/381/bmj.p978">recommending</a> the use of this vaccine, with a final decision likely to be made in July 2023. The UK drugs regulator is also considering the evidence. </p>
<p>RSV is quite closely related to measles and mumps viruses, but unlike those two, it mostly causes symptoms similar to a bad cold. It is spread through coughing and sneezing and it can hang around on surfaces for several hours. It is found all over the world, with most cases occurring <a href="https://academic.oup.com/ofid/article/8/7/ofab159/6204761">in winter</a>. </p>
<p>Healthy adults usually have fairly mild symptoms, but an RSV infection can be very serious in young children and older people. In babies and toddlers, breathing can be so badly affected that they need oxygen treatment in hospital. </p>
<p>Globally, RSV is estimated to cause <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)00478-0/fulltext">one in every 50 deaths</a> in children under five. </p>
<p>RSV is harder to diagnose in older adults but may be <a href="https://academic.oup.com/ofid/article/8/7/ofab159/6204761">more common</a> than influenza. It can develop into conditions such as pneumonia, which can be fatal. Globally, at least 300,000 people over 65 are ill enough to be admitted to hospital with an RSV infection each year, around 4% of whom will die.</p>
<figure class="align-center ">
<img alt="Older adult coughing." src="https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=412&fit=crop&dpr=1 600w, https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=412&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=412&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=517&fit=crop&dpr=1 754w, https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=517&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/525142/original/file-20230509-25-wf2cww.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=517&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">RSV can cause deadly lung disease in older adults.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/coughing-senior-man-sitting-on-sofa-615311849">Africa Studio/Shutterstock</a></span>
</figcaption>
</figure>
<h2>A long road</h2>
<p>Scientists started working on an RSV vaccine in <a href="https://www.nature.com/articles/d41586-023-01529-5?utm_source=Nature+Briefing&utm_campaign=e0b3aa1db3-briefing-dy-20230504&utm_medium=email&utm_term=0_c9dfd39373-e0b3aa1db3-42648259">the 1960s</a>. The first attempt was based on collecting whole virus grown in the laboratory and preserving it chemically so that it looked like RSV virus once inside the human body. This is a standard technique for preparing vaccines, but unfortunately it triggered an unexpected immune response. Vaccinated children reacted badly when they later picked up RSV naturally. Many ended up in hospital and <a href="https://www.nature.com/articles/d41586-021-03704-y">two sadly died</a>.</p>
<p>Researchers then tried using vaccines made against individual parts of the virus and different formulations, but <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/irv.12850">nothing seemed to work</a>. Eventually, a key part of the virus, called F protein was identified as a likely vaccine target. But making it work still proved hard, until scientists realised that the protein changed shape once the virus met the cells inside the lungs. So the trick was to <a href="https://www.nature.com/articles/d41586-021-03704-y">stabilise the F protein</a> in the vaccine so it stayed the same once it got inside the patient’s body. </p>
<p>The Arexvy vaccine, developed by the UK-based pharmaceutical company GlaxoSmithKline, is known as a “protein subunit vaccine”. It contains an artificial version of the correct format of the F protein (called RSV PreF3) plus a harmless chemical that encourages the body to take up the vaccine more easily (called an <a href="https://theconversation.com/adjuvants-the-unsung-heroes-of-vaccines-156548">adjuvant</a>).</p>
<h2>Eighty-three per cent effective</h2>
<p>In a clinical trial involving almost 25,000 volunteers, half were given Arexvy and half a placebo and they were all followed up for at least six months. The vaccine gave <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2209604">83% protection</a> against lower respiratory tract disease caused by RSV. </p>
<p>There are two forms of RSV, type A and B. The vaccine worked equally well against both types. </p>
<p>Some people did experience side-effects, but they were rare and usually minor. Serious outcomes have been found in other, smaller studies of Arexvy. In one trial, two people who were given the influenza vaccine along with Arexvy experienced <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-respiratory-syncytial-virus-rsv-vaccine">inflammation of the brain</a>. In <a href="https://www.fda.gov/news-events/press-announcements/fda-approves-first-respiratory-syncytial-virus-rsv-vaccine">another study</a>, one person developed a condition called <a href="https://www.nhs.uk/conditions/guillain-barre-syndrome/">Guillain-Barré syndrome</a>, a rare condition where the body’s immune system turns on itself and causes paralysis. Most people recover from Guillain-Barré syndrome, but it can take some time.</p>
<p>Trials are continuing to see how long the effects of the vaccine last. People usually need regular boosters for this type of vaccine, so it will probably be given annually. </p>
<p>Although RSV affects more children than adults each year, a suitable vaccine for children is not yet ready. This is because virologists still don’t fully understand how children’s immune systems interact with the virus. </p>
<p>In the meantime, children at high risk of serious illness from RSV (premature babies and those with some heart conditions) can be given palivizumab. This is not a vaccine but a laboratory-made copy of an antibody against F protein. It is a safe drug, but protection doesn’t last long and the injection has to be given once a month during RSV season.</p><img src="https://counter.theconversation.com/content/205145/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sarah Pitt 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 first vaccine against respiratory syncytial virus is 83% effective.Sarah Pitt, Principal Lecturer, Microbiology and Biomedical Science Practice, Fellow of the Institute of Biomedical Science, University of BrightonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2044192023-05-03T11:24:28Z2023-05-03T11:24:28ZThousands of unknown viruses discovered in baby poo – why this is not necessarily a bad thing<p>An international team of scientists who spent five years studying the poo of <a href="https://www.nature.com/articles/s41564-023-01345-7">647 Danish babies</a> found something astonishing. The nappy samples contained 10,000 species of virus – ten times the number of bacterial species in the same children. Most of the viruses had never been described before. </p>
<p>This may alarm many readers. Viruses haven’t exactly had a <a href="https://ourworldindata.org/covid-deaths">good reputation</a> in recent years. But what many people don’t realise is that the overwhelming majority of viruses do not make people sick and do not infect humans or animals at all. </p>
<p>The viruses I’m referring to are bacteriophages. They exclusively infect bacteria and make up a large part of the human microbiome. It’s these bacteriophages that the researchers found so abundantly in baby poo. Indeed, around 90% of the viruses found in the nappies of the Danish babies were these bacteria killers.</p>
<p>The human gut microbiome is a complex collection of microorganisms, including bacteria, archaea, microbial eukaryotes and viruses. The viral component of the gut microbiome, or virome, is mainly made up of bacteriophages that help maintain a healthy and diverse microbiome.</p>
<h2>Atlas</h2>
<p>The researchers of this new study – a collaborative team from Denmark, Canada and France – looked at how many of these 10,000 viruses were new and how best to describe all this new viral diversity in an accessible form. </p>
<p>Putting all of them in a large table would be a rather boring read. Instead, they created an “atlas of infant gut DNA virus diversity”, where they grouped the viruses into new virus families and orders based on how similar the genomes were to each other. They found 248 families of which only 16 were previously known. </p>
<p>The researchers named the remaining 232 newly identified virus families after children who took part in the study, such as Sylvesterviridae, Rigmorviridae and Tristanviridae.</p>
<p>An <a href="https://copsac.com/earlyvir/f1y/fig1.svg">interactive version</a> of the atlas is available online.</p>
<figure class="align-center ">
<img alt="Illustration of bacteriophages attacking a bacterium" src="https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=425&fit=crop&dpr=1 754w, https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=425&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/523793/original/file-20230502-1677-ej65zg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=425&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">Bacteriophages attacking a bacterium.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/3d-illustration-bacteriophage-infecting-bacterium-1126283543">Design Cells/Shutterstock</a></span>
</figcaption>
</figure>
<h2>Unique viromes</h2>
<p>What is interesting about bacteriophages and other viruses in the gut is that every person has their own unique set, with <a href="https://www.sciencedirect.com/science/article/pii/S1931312819304767">almost no overlap between two different people</a>. </p>
<p>While each gut virome is unique, it is also stable over time in adults, meaning you carry with you the same set of viruses as you age. But right after a baby is born, this virome is very different from that of an adult and it only stabilises after a couple of years. </p>
<p>When comparing the approximately 10,000 viruses of this new study with extensive reference virome collections of healthy adults, the researchers found that only about 800 of these viruses had been found before. </p>
<p>That means that when babies are born and have the first bacteriophages colonise their gastrointestinal tract, these “baby bacteriophages” don’t all stay there, but gradually get replaced with “adult bacteriophages”. </p>
<p>This replacement could be partially linked to the bacterial hosts these bacteriophages infect. For example, <em>Bacteroides</em>, <em>Faecalibacterium</em> and <em>Bifidobacterium</em> were the most prominent hosts that were predicted for the baby bacteriophages. </p>
<p>I’d like to highlight <em>Bifidobacterium</em> species here, which are very important for infant health. These bacteria help with the digestion of breastmilk and so are important early in life, but become less abundant as we age. So it makes sense that the viruses that infect <em>Bifidobacterium</em> are found more in babies and less in adults. </p>
<p>Conversely, the most abundant group of adult gut bacteriophages, members of the order <em>Crassvirales</em> were not as prevalent in baby poo, meaning children acquire these bacteriophages as they age. </p>
<p>With the addition of these 10,000 new virus species and the many new families, from just one group of several hundred Danish babies, it becomes clear that there’s more that we don’t know about the virome than what we do know. But the scientific community is working on it, one baby poo sample at a time.</p><img src="https://counter.theconversation.com/content/204419/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Evelien Adriaenssens receives funding from the Biotechnology and Biological Sciences Research Council (BBSRC) and Medical Research Council (MRC). She is affiliated with the International Committee on Taxonomy of Viruses. </span></em></p>Babies guts found to have ten times as many viral species as bacterial species.Evelien Adriaenssens, Group Leader, Gut viruses & Viromics, Quadram InstituteLicensed as Creative Commons – attribution, no derivatives.