tag:theconversation.com,2011:/au/topics/immunity-462/articlesImmunity – The Conversation2024-03-29T08:28:37Ztag:theconversation.com,2011:article/2131972024-03-29T08:28:37Z2024-03-29T08:28:37ZGut microbiome: meet Klebsiella pneumoniae – an opportunistic pathogen that is harmless to some, but causes severe disease in others<figure><img src="https://images.theconversation.com/files/585005/original/file-20240328-22-5pw785.jpg?ixlib=rb-1.1.0&rect=0%2C8%2C5490%2C3649&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">_K pneumoniae_ is the most common cause of hospital-aquired pneumonia. </span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/klebsiella-pneumoniae-colonies-close-media-plate-1280636989">AnaLysiSStudiO/ Shutterstock</a></span></figcaption></figure><p><em>Klebsiella pneumoniae</em> is a common species of bacteria found in our bodies – and may even be lurking in your gut, mouth or nose right now. But it’s also a notoriously harmful bacteria that can make us very ill. </p>
<p>It’s the most common cause of <a href="https://www.ncbi.nlm.nih.gov/books/NBK519004/">hospital-acquired pneumonia</a> in the US and the second most frequent cause of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3150015/">urinary tract infections</a> worldwide, after <em>Escherichia coli</em> (<em>E coli</em>). If it infects wounds or enters the bloodstream, <em>K pneumoniae</em> can cause <a href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1011233">bloodstream infections and sepsis</a>.</p>
<p>So how can <em>K pneumoniae</em> live harmlessly among the rest of the microbiome in some of us, yet cause disease in others? Understanding this may hold the key to preventing infections.</p>
<p>Scientists aren’t entirely sure what proportion of the population carries <em>K pneumoniae</em> as part of their normal gut microbiome. Past attempts have had highly variable results.</p>
<p>For example, one survey of healthy people detected <em>K pneumoniae</em> in <a href="https://pubmed.ncbi.nlm.nih.gov/23071716/">almost 4% of stool samples</a>. Yet other studies show <em>K pneumoniae</em> is noticeably more common among certain groups – including <a href="https://pubmed.ncbi.nlm.nih.gov/29340588/">hospital patients</a>, people living in <a href="https://pubmed.ncbi.nlm.nih.gov/32404021/">lower income countries</a> and, in particular, among people who had travelled to <a href="https://aricjournal.biomedcentral.com/articles/10.1186/s13756-018-0429-7">Asia</a>. </p>
<p><em>K pneumoniae</em> is what’s known as an opportunistic pathogen. This means that when carried in the gut, nose or mouth as part of the normal microbiota, <em>K pneumoniae</em> should not cause any health problems unless a person’s immune system becomes compromised due to an infection or disease. So our microbiome can act as a reservoir of <em>K pneumoniae</em>, from which it can spread to other parts of the body and cause infection.</p>
<p><a href="https://academic.oup.com/cid/article/65/2/208/3084729?login=true">One study</a> of 498 intensive care patients at a hospital in Australia found that half of <em>K pneumoniae</em> infections were caused by the patient’s own <em>K pneumoniae</em> strain that had already been living in their gut or throat.</p>
<p>It’s thought that <em>K pneumoniae</em> can spread from the gut to other parts of the body via medical devices such as <a href="https://journals.asm.org/doi/10.1128/spectrum.00641-23">ventilators</a>. This type of gut-to-lung translocation has recently been observed in other pneumonia-causing species of bacteria, such as <em><a href="https://www.nature.com/articles/s41467-022-34101-2">Pseudomonas aeruginosa</a></em>. Surgeries can also make possible the spread of <em>K pneumoniae</em> to sites where it can cause infection. </p>
<h2>Stopping the spread</h2>
<p>Unfortunately, some <em>K pneumoniae</em> strains have developed <a href="https://bmcmicrobiol.biomedcentral.com/articles/10.1186/s12866-023-02974-y">high levels of drug resistance</a>. This means that some drugs once used to treat <em>K pneumoniae</em> infections now no longer work. </p>
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<img alt="A digital rendering of how Klebsiella pneumoniae would look under a microscope." src="https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/585008/original/file-20240328-16-fxidcb.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Some strains of <em>Klebsiella pneumoniae</em> have increasingly become resistant to the drugs designed to kill them.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/bacteria-klebsiella-3d-illustration-gramnegative-rodshaped-584511661">Kateryna Kon/ Shutterstock</a></span>
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<p>It’s particularly concerning that some strains of <em>K pneumoniae</em> are developing resistance to the group of antibiotics called carbapenems, which are generally only used as a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3195018/">last resort</a> treatment when other antibiotics haven’t worked. And, this resistance is becoming more widespread among the population.</p>
<p>There’s an <a href="https://www.who.int/news/item/27-02-2017-who-publishes-list-of-bacteria-for-which-new-antibiotics-are-urgently-needed">urgent need</a> to develop alternatives to antibiotics so that cases of drug-resistant <em>K pneumoniae</em> can be prevented or treated. Our laboratory’s research focuses on harnessing the gut microbiome as a potential solution. </p>
<p>Since carrying <em>K pneumoniae</em> in the gut is a known <a href="https://pubmed.ncbi.nlm.nih.gov/28369261/">risk factor</a> for subsequent infection, one route to avoiding this could be to manipulate the microbiome. This could be done by using probiotics containing beneficial species of bacteria to limit <em>K pneumoniae</em> in the gut. Such a solution could be especially important for people in hospitals or care homes, where <em>K pneumoniae</em> is more <a href="https://pubmed.ncbi.nlm.nih.gov/23770266/">prevalent</a> and infection risk is highest.</p>
<p>The microbiome has long been known to provide a host with a degree of natural protection against infection via a property known as <a href="https://www.nature.com/articles/s41579-022-00833-7">colonisation resistance</a>. This is when resident gut bacteria outcompete incoming species, including potential pathogens, and prevent them from establishing in the gut. </p>
<p>But microbiomes <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428241/">vary greatly</a> – and some people carry more protective microbial communities than others.</p>
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<strong>
Read more:
<a href="https://theconversation.com/diverse-gut-microbiomes-give-better-protection-against-harmful-bugs-now-we-know-why-219734">Diverse gut microbiomes give better protection against harmful bugs – now we know why</a>
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<p>My colleagues and I wanted to understand why some gut communities can resist the growth of harmful bacteria while others cannot. In the lab, we combined human gut bacteria into communities containing different diversities and compositions of bacterial species. We then challenged these communities with <em>K pneumoniae</em> (as well as other harmful bacteria, such as <em>Salmonella</em>). </p>
<p>We found that <a href="https://www.science.org/doi/epdf/10.1126/science.adj3502">diverse gut microbiomes</a> were more protective against <em>K pneumoniae</em> colonisation. We showed that this protection was due to the resident gut bacteria using up the nutrients needed in order for invading microbes to grow. This led us to develop a way of predicting combinations of gut bacteria that can resist growth of unwanted species of bacteria such as <em>K pneumoniae</em>. </p>
<p>We are still only just beginning to understand the role that microbes play when it comes to our health. Some of these microbes, such as <em>K pneumoniae</em>, can even be harmful and harmless at the same time. Studying the interactions between the members of the gut microbiota is a critical area of research for microbiome scientists because it could lead to new ways of preventing or treating infections. </p>
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<p><em>This article is part of <a href="https://theconversation.com/uk/topics/meet-your-gut-microbes-150943?utm_source=InArticleTop&utm_medium=TCUK&utm_campaign=Health2024">Meet Your Gut Microbes</a>, a series about the rich constellation of bacteria, viruses, archaea and fungi that live in people’s digestive tracts. Scientists are increasingly realising their importance in shaping our health – both physical and mental. Each week we will look at a different microbe and bring you the most up-to-date research on them.</em></p>
<hr><img src="https://counter.theconversation.com/content/213197/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Frances Spragge receives funding from The Wellcome Trust. </span></em></p>Some strains of this opportunistic pathogen are also increasingly becoming resistant to the drugs designed to treat them.Frances Spragge, Postdoctoral Researcher in Microbiology, University of OxfordLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2139262024-02-23T12:57:17Z2024-02-23T12:57:17ZGut microbiome: meet Lactobacillus acidophilus – the gut health superhero<figure><img src="https://images.theconversation.com/files/577544/original/file-20240223-24-46adyy.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C5176%2C3445&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Eating yoghurt is one way of getting more _Lactobacillus acidophilus_ into your diet.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-woman-home-eating-yogurt-111275633">Josep Suria/ Shutterstock</a></span></figcaption></figure><p>Your gut is like a bustling city of trillions of microscopic inhabitants – including bacteria. While some of these bacterial inhabitants are villains, causing illness, infection and disease, others are good – supporting our health and keeping things running smoothly. </p>
<p>But one species of bacterium in our gut is so good and does so much for our health, that it might well be compared to a gut superhero. This microbe goes by the name of <em><a href="https://www.cabdirect.org/cabdirect/abstract/19352701869">Lactobacillus acidophilus</a></em>. </p>
<p><em>Lactobacillus acidophilus</em> might sound like a mouthful, but don’t let its long name intimidate you. In simple terms, it’s a tiny bacterium that belongs to a group of microorganisms known for their <a href="https://pubmed.ncbi.nlm.nih.gov/24912386/">probiotic properties</a> – meaning it provides health benefits when consumed in adequate quantities.</p>
<p>This microbe hangs out in your gut (mainly your small intestine) and helps keep things running smoothly. In fact, <em>Lactobacillus acidophilus</em> has an incredible number of important functions.</p>
<p>It acts as a digestion buddy, munching on things you can’t digest entirely – such as certain sugars and fibres. For example, it helps digest foods rich in lactose (such as dairy products like milk, yogurt and cheese), as well as fermentable carbohydrates found in vegetables, fruits and grains. By doing so, <a href="https://pubmed.ncbi.nlm.nih.gov/30468509/">it helps break down your food</a>, making it easier for your body to absorb nutrients.</p>
<p>Since your gut is a delicate ecosystem, <em>Lactobacillus acidophilus</em> plays a crucial role in maintaining the right balance of bacteria by <a href="https://pubmed.ncbi.nlm.nih.gov/22254077/">preventing harmful bacteria</a> from taking over and causing trouble.</p>
<p>This microbe also <a href="https://pubmed.ncbi.nlm.nih.gov/23372900/">strengthens your body’s defence system</a>. It does this by helping your immune cells <a href="https://pubmed.ncbi.nlm.nih.gov/20823239/">communicate better</a> and stay alert so they’re ready to fight off invaders. </p>
<p>And when your stomach is upset or you’re stressed, <em>Lactobacillus acidophilus</em> is the microbe that comes to the rescue, soothing irritation and <a href="https://pubmed.ncbi.nlm.nih.gov/16728323/">helping ease digestive discomfort</a>.</p>
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<img alt="A man holds his stomach in pain." src="https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/577545/original/file-20240223-20-cu5btb.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">One of the benefits this microbe has is easing digestive problems.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/man-suffering-stomach-ache-sitting-on-488527312">Antonio Guillem/ Shutterstock</a></span>
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<p>All of these important functions mean <em>Lactobacillus acidophilus</em> is a true friend to your body, and its affects on your health are pretty impressive, with benefits such as:</p>
<ul>
<li><strong>Happy tummies:</strong> By maintaining a balanced gut environment, your stomach will feel <a href="https://pubmed.ncbi.nlm.nih.gov/18274900/">more comfortable</a>, and you have less chance of experiencing tummy troubles such as <a href="https://pubmed.ncbi.nlm.nih.gov/16728323/">diarrhoea</a>, constipation and bloating.</li>
<li><strong>Immune support:</strong> By keeping your gut in tip-top shape, <em>Lactobacillus acidophilus</em> <a href="https://pubmed.ncbi.nlm.nih.gov/19651563/">helps protect you</a> from infections and illnesses. It’s shown to be particularly good at keeping <a href="https://pubmed.ncbi.nlm.nih.gov/23594927/">influenza</a> at bay. </li>
<li><strong>Controlling allergies and inflammation:</strong> Some studies suggest that having a strong colony of <em>Lactobacillus acidophilus</em> in your gut might <a href="https://pubmed.ncbi.nlm.nih.gov/19840300/">reduce the risk of allergies</a> and <a href="https://pubmed.ncbi.nlm.nih.gov/24954372/">inflammation-related conditions</a> (such as eczema). It acts like a natural shield against <a href="https://pubmed.ncbi.nlm.nih.gov/26044853/">sneezing fits and sore joints</a>.</li>
<li><strong>Preserving mental wellbeing:</strong> Believe it or not, your gut health can influence your mood. <em>Lactobacillus acidophilus</em> might play a role in <a href="https://pubmed.ncbi.nlm.nih.gov/29521671/">promoting good mental wellbeing</a>.</li>
</ul>
<p>Given all the important roles that <em>Lactobacillus acidophilus</em> plays in your health, if you’re keen to fill your gut with this microbe you can find it in tasty fermented foods such as <a href="https://www.tandfonline.com/doi/abs/10.1080/10408398.2011.621169?casa_token=q5rNmHVBFjAAAAAA:79FQSbhMoQYMVxrw_WvyFaeHmSR50olvQO8JaGY9ZzluOnYAy_CLWaJhx6J8utAb1F6xgl60gYRN8w">yogurt and kefir</a>. </p>
<h2>A deeper look</h2>
<p>Even though we know a lot about <em>Lactobacillus acidophilus</em>, there’s still much to explore. Scientists are currently digging deeper to understand whether there are <a href="https://pubmed.ncbi.nlm.nih.gov/16875422/">different strains of this microbe</a> – and if each of these strains have unique abilities. </p>
<p>Scientists are also working on tailoring probiotics to a person’s specific needs. Imagine having a <a href="https://www.nature.com/articles/s41564-020-0721-1">personalised probiotic</a> superhero designed just for you. People with inflammatory bowel disease, weakened immune systems, allergies and mental health concerns may benefit from personalised products containing probiotic strains such as <em>Lactobacillus acidophilus</em>, because of the benefits it may have for these issues. </p>
<p>And finally, researchers are continuing to investigate the link between gut health and the brain – with scientists taking a particular interest in investigating how specifically <em>Lactobacillus acidophilus</em> might influence <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6445894/">mood and mental wellbeing</a>.</p>
<p><em>Lactobacillus acidophilus</em> is a tiny but mighty superhero in your gut, working hard to keep you healthy and happy. So the next time you enjoy <a href="https://www.tandfonline.com/doi/abs/10.1080/10408398.2011.621169?casa_token=q5rNmHVBFjAAAAAA:79FQSbhMoQYMVxrw_WvyFaeHmSR50olvQO8JaGY9ZzluOnYAy_CLWaJhx6J8utAb1F6xgl60gYRN8w">a yogurt or sip on some kefir</a>, think of it as giving your friendly gut superhero a high-five. </p>
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<p><em>This article is part of <a href="https://theconversation.com/uk/topics/meet-your-gut-microbes-150943?utm_source=InArticleTop&utm_medium=TCUK&utm_campaign=Health2024">Meet Your Gut Microbes</a>, a series about the rich constellation of bacteria, viruses, archaea and fungi that live in people’s digestive tracts. Scientists are increasingly realising their importance in shaping our health – both physical and mental. Each week we will look at a different microbe and bring you the most up-to-date research on them.</em></p>
<hr><img src="https://counter.theconversation.com/content/213926/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>Fermented foods, such as yoghurt and kefir, are great sources of this immune-boosting microbe.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/2213982024-01-23T06:51:20Z2024-01-23T06:51:20ZHow long does immunity last after a COVID infection?<figure><img src="https://images.theconversation.com/files/570785/original/file-20240123-17-tcgvhd.jpg?ixlib=rb-1.1.0&rect=8%2C0%2C5529%2C3686&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/adult-man-lies-on-couch-home-1946857264">Kazantseva Olga/Shutterstock</a></span></figcaption></figure><p>Nearly four years into the pandemic, Australia, like many other countries, is still seeing large numbers of <a href="https://nindss.health.gov.au/pbi-dashboard/">COVID cases</a>. Some 860,221 infections were recorded around the country in 2023, while 30,283 cases have already been reported in 2024. </p>
<p>This is likely to be a significant underestimate, with fewer people testing and reporting than earlier in the pandemic. But the signs suggest parts of Australia are experiencing yet <a href="https://www.abc.net.au/news/2024-01-23/covid-19-case-numbers-from-australia-states-and-territories/103374656">another COVID surge</a>. </p>
<p>While some lucky people claim to have never had COVID, many are facing our second, third or even fourth infection, often despite having been vaccinated. You might be wondering, how long does immunity last after a previous infection or vaccination?</p>
<p>Let’s take a look at what the evidence shows.</p>
<h2>B cells and T cells</h2>
<p>To answer this question, we need to understand a bit about how <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">immunity</a> to SARS-CoV-2 (the virus that causes COVID) works. </p>
<p>After being infected or vaccinated, the immune system develops specific antibodies that can neutralise SARS-CoV-2. B cells remember the virus for a period of time. In addition, the immune system produces memory T cells that can kill the virus, and remain in the blood for some months after the clearance of the infection or a vaccination.</p>
<p>A <a href="https://www.science.org/doi/full/10.1126/science.abf4063?rfr_dat=cr_pub++0pubmed&url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org">2021 study</a> found 98% of people had antibodies against SARS-CoV-2’s spike protein (a protein on the surface of the virus that allows it to attach to our cells) one month after symptom onset. Six to eight months afterwards, 90% of participants still had these neutralising antibodies in their blood.</p>
<p>This means the immune system should have recognised and neutralised the same SARS-CoV-2 variant if challenged within six to eight months (if an infection occurred, it should have resulted in mild to no symptoms).</p>
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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>
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<h2>But what about when the virus mutates?</h2>
<p>As we know, SARS-CoV-2 has mutated over time, leading to the emergence of new variants such as alpha, beta, delta and omicron. Each of these variants carries mutations that are new to the immune system, even if the person has been previously infected with an earlier variant. </p>
<p>A new variant likely won’t be <a href="https://www.science.org/doi/10.1126/science.adj0070">perfectly recognised</a> – or even <a href="https://www.cell.com/cell/pdf/S0092-8674(21)01578-6.pdf">recognised at all</a> – by the already activated memory T or B cells from a previous SARS-CoV-2 infection. This could explain why people can be so readily reinfected with COVID.</p>
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<img alt="A close up of a person performing a RAT." src="https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/570803/original/file-20240123-21-9mk3k7.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">COVID reinfections are common.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/close-person-using-coronavirus-covid19-rapid-1969543405">Ink Drop/Shutterstock</a></span>
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<p>A recent <a href="https://www.thelancet.com/article/S0140-6736(22)02465-5/fulltext#seccestitle10">review of studies</a> published up to the end of September 2022 looked at the protection conferred by previous SARS-CoV-2 infections.</p>
<p>The authors found a previous infection provided protective immunity against reinfection with the ancestral, alpha, beta and delta variants of 85.2% at four weeks. Protection against reinfection with these variants remained high (78.6%) at 40 weeks, or just over nine months, after the previous infection. This protection decreased to 55.5% at 80 weeks (18 months), but the authors noted there was a lack of data at this time point. </p>
<p>Notably, an earlier infection provided only 36.1% protection against a reinfection with omicron BA.1 at 40 weeks. Omicron has been described as an <a href="https://www.nature.com/articles/s41564-022-01143-7">immune escape variant</a>.</p>
<p>A prior infection showed a high level of protection against severe disease (above 88%) up to 40 weeks regardless of the variant a person was reinfected with.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/there-are-still-good-reasons-to-avoid-catching-covid-again-for-one-your-risk-of-long-covid-goes-up-each-time-196041">There are still good reasons to avoid catching COVID again – for one, your risk of long COVID goes up each time</a>
</strong>
</em>
</p>
<hr>
<h2>What about immunity after vaccination?</h2>
<p>So far almost 70 million COVID vaccines <a href="https://www.health.gov.au/topics/covid-19/reporting">have been administered</a> to more than <a href="https://www.health.gov.au/resources/publications/covid-19-vaccine-rollout-update-12-january-2023?language=en">22 million people</a> in Australia. Scientists estimated COVID vaccines prevented around <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(22)00320-6/fulltext">14.4 million deaths</a> in 185 countries in the first year after they became available.</p>
<p>But we know COVID vaccine effectiveness wanes over time. A <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2804451?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=050323">2023 review</a> found the original vaccines were 79.6% and 49.7% effective at protecting against symptomatic delta infection at one and nine months after vaccination respectively. They were 60.4% and 13.3% effective against symptomatic omicron at the same time points.</p>
<p>This is where booster doses come into the picture. They’re important to keep the immune system ready to fight off the virus, particularly for those who are more vulnerable to the effects of a COVID infection. </p>
<p>Plus, regular booster doses can provide immunity against different variants. COVID vaccines are constantly being <a href="https://mvec.mcri.edu.au/references/covid-19/">reviewed and updated</a> to ensure optimal protection against <a href="https://www.who.int/activities/tracking-SARS-CoV-2-variants">current circulating strains</a>, with the latest shot available designed to target <a href="https://www.health.gov.au/ministers/the-hon-mark-butler-mp/media/new-covid-19-vaccines-available-to-target-current-variants">the omicron variant XBB 1.5</a>. This is similar to how we approach seasonal flu vaccines.</p>
<figure class="align-center ">
<img alt="A woman coughing at her desk." src="https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/570795/original/file-20240123-19-6v7f8u.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">COVID immunity wanes over time – both from infection and vaccination.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/sick-african-american-girl-working-home-1109017139">Diego Cervo/Shutterstock</a></span>
</figcaption>
</figure>
<p>A <a href="https://www.nature.com/articles/s41598-023-50335-6">recent study</a> showed a COVID vaccination provides longer protection against reinfection than natural protection alone. The median time from infection to reinfection in non-vaccinated people was only six months, compared with 14 months in people who had received one, two or three doses of vaccine after their first infection. This is called <a href="https://www.science.org/doi/10.1126/science.abj2258">hybrid immunity</a>, and other research has similarly found it provides better protection than natural infection alone.</p>
<p>It also seems timing is important, as receiving a vaccine too soon after an infection (less than six months) appears to be <a href="https://www.nature.com/articles/s41598-023-50335-6">less effective</a> than getting vaccinated later.</p>
<h2>What now?</h2>
<p>Everyone’s immune system is slightly unique, and SARS-CoV-2 continues to mutate, so knowing exactly how long COVID immunity lasts is complicated. </p>
<p>Evidence suggests immunity following infection should generally last six months in healthy adults, and can be prolonged with vaccination. But there are exceptions, and all of this assumes the virus has not mutated so much that it “escapes” our immune response.</p>
<p>While many people feel the COVID pandemic is over, it’s important we don’t forget the lessons we have learned. Practices such as wearing a mask and staying home when unwell can reduce the spread of many viruses, not only <a href="https://www.bmj.com/content/375/bmj-2021-068302">COVID</a>.</p>
<p>Vaccination is not mandatory, but for older adults eligible for a booster under the <a href="https://www.health.gov.au/news/atagi-update-on-the-covid-19-vaccination-program">current guidelines</a>, it’s a very good idea.</p><img src="https://counter.theconversation.com/content/221398/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>While some lucky people believe they’ve never had COVID, many are facing their second, third or even fourth infection. Here’s what the evidence shows.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/2205802024-01-08T19:02:22Z2024-01-08T19:02:22ZTrump’s arguments for immunity not as hopeless as some claim<figure><img src="https://images.theconversation.com/files/568063/original/file-20240105-27-bf9x5s.jpg?ixlib=rb-1.1.0&rect=20%2C0%2C6689%2C4476&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Donald Trump has claimed that presidents are immune from prosecution for official acts.</span> <span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/TrumpCapitolRiotHarassment/8742cb120b814b02a1475cc58dfd3e9f/photo">AP Photo/Toby Brusseau</a></span></figcaption></figure><p>Former President Donald Trump’s claims of immunity from criminal prosecution will be argued before the U.S. Court of Appeals for the District of Columbia Circuit on Jan. 9, 2024 – on an <a href="https://www.law.cornell.edu/wex/interlocutory_appeal">interlocutory appeal</a> from his trial for election interference. His arguments have been <a href="https://www.nytimes.com/2023/12/01/us/politics/trump-chutkan-immunity.html">rejected by a district court judge</a>, and the Supreme Court has <a href="https://www.cbsnews.com/news/supreme-court-declines-to-fast-track-trump-immunity-dispute-in-blow-to-special-counsel/">declined to weigh in</a> – for now. </p>
<p>Commentators have described his immunity arguments as “<a href="https://www.theguardian.com/us-news/2024/jan/01/donald-trump-legal-problems-ex-president-strategy">frivolous</a>” and “<a href="https://www.msnbc.com/opinion/msnbc-opinion/donald-trump-immunity-claim-rcna119695">absurd</a>.” But such accounts underestimate the arguments’ weight and at times misconstrue them. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A bearded man in a coat and tie stands in front of an American flag." src="https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/568064/original/file-20240105-27-2phosz.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">Special counsel Jack Smith is leading the federal prosecutions against former President Donald Trump.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/TrumpCapitolRiot/e5bdeb21b0e84ddf9dd175e866831b32/photo">AP Photo/J. Scott Applewhite</a></span>
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</figure>
<h2>A related absolute immunity already exists</h2>
<p>Trump claims he is immune from <a href="https://www.justice.gov/storage/US_v_Trump_23_cr_257.pdf">federal charges on seeking to overturn the 2020 elections</a>.</p>
<p>His first line of defense claims that his actions are covered by a constitutional immunity protecting presidents when they act in their official capacity. Trump’s lawyers are not claiming that he couldn’t be prosecuted for, say, <a href="https://www.npr.org/sections/thetwo-way/2016/01/23/464129029/donald-trump-i-could-shoot-somebody-and-i-wouldnt-lose-any-voters">shooting a pedestrian on 5th Avenue</a>. They are saying he can’t be prosecuted for so-called “official acts.”</p>
<p>A related immunity has been recognized in the past. </p>
<p>In 1982, the Supreme Court recognized that presidents have absolute immunity from civil lawsuits for their official actions. The principal rationale for this immunity was to allow the president “<a href="https://supreme.justia.com/cases/federal/us/457/731/">maximum ability to deal fearlessly and impartially with the duties of his office</a>.” The case described the president as “<a href="https://supreme.justia.com/cases/federal/us/457/731/">the officeholder [who] must make the most sensitive and far-reaching decisions</a> entrusted to any official under our constitutional system,” and held that the Constitution ensured he was not “<a href="https://supreme.justia.com/cases/federal/us/457/731/">unduly cautious in the discharge of his official duties</a>.” Presidents should not take official actions with the fear of civil liability hanging over their heads.</p>
<p>The question remained whether a president could be criminally charged for his official actions.</p>
<p>Trump claims he cannot. He argues that just as the Constitution protects presidents from civil lawsuits, it also protects them from criminal charges – and for an analogous reason: preserving the president’s ability to make official decisions free from the fear of criminal prosecution. </p>
<p>The brief of special counsel Jack Smith responded that it is actually <a href="https://storage.courtlistener.com/recap/gov.uscourts.cadc.40415/gov.uscourts.cadc.40415.1208583920.0_1.pdf">good if presidents are worried about possible criminal liability</a>. Moreover, while immunity to civil liability makes sense, because civil lawsuits can be filed by practically everyone and for myriads of petty reasons, criminal charges usually relate to weightier concerns, and their filings involve various checks and balances. </p>
<p>Nevertheless, it is conceivable that courts would recognize presidential criminal immunity for official acts. If they do, the question would become how to define “official acts,” and whether the actions forming the basis for Trump’s charges, which include <a href="https://apnews.com/article/donald-trump-investigation-2024-joe-biden-05d0d0d7a0adbec796caecdc6862588b">many interactions with state and federal officials</a>, qualify under that definition. It seems reasonable to believe that many of them do not and are better described as the acts of a candidate seeking reelection. But some of these acts might qualify. </p>
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<h2>The complication from the impeachment clauses</h2>
<p>Yet, the argument for absolute criminal immunity faced a preliminary hurdle: <a href="https://constitution.congress.gov/constitution/article-1/#article-1-section-3-clause-7">Article 1, Section 3, of the U.S. Constitution</a> states that while “Judgment in Cases of Impeachment shall not extend further than to removal from Office … the Party convicted shall nevertheless be liable and subject to Indictment, Trial, Judgment and Punishment, according to Law.” In other words, the Constitution explicitly contemplates the criminal prosecution of a president.</p>
<p>As a brief by the special counsel put it, “<a href="https://storage.courtlistener.com/recap/gov.uscourts.dcd.258149/gov.uscourts.dcd.258149.109.0.pdf">the Impeachment Judgment Clause entirely undermines the defendant’s claim</a> that a former president’s immunity from criminal prosecution should be ‘absolute’ … because a former president who has been impeached and convicted will be liable to criminal prosecution.”</p>
<p>Trump’s response conceded that convicted presidents could indeed face criminal charges for their official acts. But he went on to claim that since he was acquitted – only <a href="https://www.cnn.com/2021/02/13/politics/senate-impeachment-trial-day-5-vote/index.html">57 senators voted to convict him</a>, short of the 67 needed – he was not liable for criminal prosecution. </p>
<p>Trump’s response became the subject of much disparagement. The New York Times called it an “<a href="https://www.nytimes.com/2024/01/02/us/politics/trump-appeals-court-immunity.html">even more audacious argument</a>” than his claim of absolute immunity. But some of that criticism derives from an uncharitable interpretation of Trump’s claims. </p>
<p>Some critics construed the claim to mean that all officials who are subject to impeachment proceedings – which include “<a href="https://constitution.congress.gov/constitution/article-2/#article-2-section-4">The President, Vice President and all Civil Officers of the United States</a>” – could not face criminal charges for official acts unless they were first impeached and convicted of them. </p>
<p>A group of former government officials and constitutional lawyers wrote in a legal brief that Trump’s argument “<a href="https://democracy21.org/wp-content/uploads/2023/12/23-3228-Amici-Br.-of-Former-Govt-Officials-and-Constitutional-Lawyers-No.-23-3228-DC-Cir.pdf">would permit countless officials to evade criminal liability</a>.” They went on to say, “Such an outcome would … contradict decades of practice in which the Executive Branch has prosecuted, and the Judicial Branch has convicted, civil officers for crimes committed while in office – regardless of whether they were first convicted in an impeachment trial.” The special counsel made <a href="https://storage.courtlistener.com/recap/gov.uscourts.cadc.40415/gov.uscourts.cadc.40415.1208583920.0_1.pdf">similar objections</a>. </p>
<p>Indeed, impeachment proceedings are <a href="https://www.loc.gov/nls/new-materials/book-lists/the-history-of-impeachment/">very rare</a>, and most eligible offenders never face an impeachment. Moreover, as the critics point out, criminal acts may be discovered after the person in question has already left office. </p>
<p>But these strike me as straw-man arguments. Trump’s claim that a president must be impeached and convicted before he can be criminally liable for official acts is premised on the background absolute immunity Trump has claimed for the presidency. To quote from Trump’s brief before the district court: “<a href="https://s3.documentcloud.org/documents/24015079/trump-motion-to-dismiss.pdf">President Trump was acquitted</a> … after trial in the Senate, and he thus remains immune from prosecution.” </p>
<p>The key word is “remains” because, in Trump’s argument, the impeachment clause provides an exception to the alleged background presidential immunity: Presidents are criminally immune for their official actions, unless they are impeached and convicted for them. In other words, nothing in Trump’s argument prevents the criminal indictment of civil officers who have not been impeached at all, because they do not enjoy absolute criminal immunity to begin with.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A view of a formal legislative chamber with many people standing at their desks and on a dais." src="https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/568065/original/file-20240105-14-smb533.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"></a>
<figcaption>
<span class="caption">Members of the U.S. Senate are sworn in Jan. 26, 2021, before beginning the second impeachment trial of Donald Trump.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/CongressExplainingTrumpImpeachmentTrial/ee7eea151da8428e99603baf2320052f/photo">Senate Television via AP</a></span>
</figcaption>
</figure>
<h2>Does acquittal in an impeachment proceeding create or preserve criminal immunity?</h2>
<p>In his late briefs, Trump adds a second line of defense: He claims that his impeachment acquittal independently forestalls his criminal trial because of the ban on <a href="https://constitution.congress.gov/constitution/amendment-5/">“double jeopardy</a>.” That claim, if upheld, would provide Trump with criminal immunity whether presidents enjoy absolute immunity or not. The claim would work only if Trump’s impeachment and his criminal prosecution were based on the same acts – an allegation that is disputed by the special counsel. </p>
<p>But the claim, in any case, is weak and at odds with some other statements Trump’s briefs make. Indeed, since impeachment proceedings are <a href="https://www.govinfo.gov/content/pkg/CPRT-116HPRT38513/html/CPRT-116HPRT38513.htm">not limited to official acts</a>, accepting Trump’s double jeopardy argument would mean that a president could also become immune for unofficial criminal conduct – such as shooting a pedestrian on 5th Avenue – if he were impeached for that act but acquitted. </p>
<p>That argument proves too much, and would also be at odds with then-President Bill Clinton’s agreement to a five-year suspension of his Arkansas law license in a <a href="https://www.nytimes.com/2001/01/19/politics/clinton-reaches-deal-to-avoid-indictment-to-give-up-law-license.html">settlement aimed at preventing his subsequent criminal prosecution for perjury</a> – even though he was acquitted in the <a href="https://guides.loc.gov/federal-impeachment/bill-clinton">impeachment proceeding for that unofficial act</a>.</p>
<p>The stronger version of Trump’s impeachment clauses argument presumes the president’s absolute immunity for official acts. Here, Trump acknowledges that an impeachment conviction removes that protection – but insists that an acquittal does not. That is why Trump’s brief states, “<a href="https://www.washingtonpost.com/documents/f25cf425-77ad-4524-8101-fdfabc62ecd7.pdf">A former President is subject to criminal process for his unofficial conduct</a>; and he is subject to criminal prosecution for official acts for which he has been impeached and convicted.” Against a background of absolute immunity, Trump’s impeachment clauses argument is not unreasonable.</p>
<p>It all sounds a bit complicated, but the ensuing conclusion is simple: The impeachment clauses debate is a sideshow. The principal action in this appeal is whether presidents have absolute criminal immunity for official acts. </p>
<p><a href="https://www.newsweek.com/donald-trump-indictment-joe-biden-truth-social-1839004">In our present political culture</a>, Trump’s arguments for criminal immunity – and his corollary take on the impeachment clauses – may be seen by some judges and justices as stronger than some critics anticipate.</p><img src="https://counter.theconversation.com/content/220580/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Ofer Raban does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The former president has raised several legal arguments that do not yet have clear answers. A constitutional scholar says they’re questions worth asking.Ofer Raban, Professor of Constitutional Law, University of OregonLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2152172023-11-20T13:18:45Z2023-11-20T13:18:45ZImmune health is all about balance – an immunologist explains why both too strong and too weak an immune response can lead to illness<figure><img src="https://images.theconversation.com/files/559704/original/file-20231115-15-wutiiv.png?ixlib=rb-1.1.0&rect=0%2C0%2C2044%2C1593&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">When immune cells become overactive, your immune system itself can cause disease.</span> <span class="attribution"><a class="source" href="https://flic.kr/p/2oHpNSe">NIAID/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span></figcaption></figure><p>For immune health, some influencers seem to think the Goldilocks philosophy of “just right” is overrated. Why settle for less immunity when you can have more? Many social media posts push supplements and other life hacks that “boost your immune system” to keep you healthy and fend off illness.</p>
<p>However, these claims are not based on science and what is known about immune function. Healthy immune systems don’t need to be “boosted.” Instead, the immune system works best when it is <a href="https://doi.org/10.1038/ni.2430">perfectly balanced</a>. Scientific experts on the immune system – immunologists – know that too much of an immune reaction could result in allergies, autoimmune disorders or <a href="https://theconversation.com/what-is-inflammation-two-immunologists-explain-how-the-body-responds-to-everything-from-stings-to-vaccination-and-why-it-sometimes-goes-wrong-193503">chronic inflammation</a>. On the flip side, <a href="https://theconversation.com/immunocompromised-people-make-up-nearly-half-of-covid-19-breakthrough-hospitalizations-an-extra-vaccine-dose-may-help-166241">too little of an immune reaction</a> could result in illness or infection.</p>
<p>Your immune system requires a delicate balance to operate properly. When it’s out of balance, your immune system itself can cause disease.</p>
<h2>Cellular balance</h2>
<p>The immune system is the mobile defense system of your body. It is a complex network of cells and organs that work together to protect your body from infection and disease. Your immune cells are continually on patrol, traveling throughout your body looking for infectious invaders and damage. </p>
<p>New immune cells are created in your bone marrow. Certain immune cells – called <a href="https://theconversation.com/coronavirus-b-cells-and-t-cells-explained-141888">B and T cells</a> – are the special forces of the immune system, playing an important role in the elimination of infectious invaders. Because of this role, these cells undergo a rigorous boot camp during their development to ensure they will not discharge friendly fire on healthy cells in the body. </p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/PSRJfaAYkW4?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Your immune system is an extensive network of cells and many other components that constantly surveil your body.</span></figcaption>
</figure>
<p>Any <a href="https://doi.org/10.1038/nri.2017.19">B cell</a> or <a href="https://doi.org/10.1146/annurev-immunol-101320-022432">T cell</a> exhibiting activity against the self – or autoreactivity – is killed during training. Millions of newly created B and T cells are killed every day because they fail this training process. If these self-reactive cells escape destruction, they could turn against the body and carry out an inappropriate <a href="https://doi.org/10.1038/ni.3731">autoimmune attack</a>. </p>
<p><a href="https://scholar.google.com/citations?view_op=list_works&hl=en&hl=en&user=PGIEO34AAAAJ">My research</a> investigates how B cells are able to slip past the checkpoints the immune system has in place to guard against autoreactivity. These <a href="https://doi.org/10.1172/jci12462">tolerance checkpoints</a> ensure that autoreactive immune cells are either purged from the body or held in permanent lockdown and unable to engage in inappropriate responses that would target healthy tissue.</p>
<h2>More isn’t necessarily better</h2>
<p>You’ve likely seen advertisements for dietary supplements that promise to “boost immune function.” While this may sound appealing, it is important to keep in mind that the immune system functions best when perfectly balanced.</p>
<p>If the immune system is like a thermostat, turning it up too high results in overactivation and uncontrolled inflammation, while turning it down too low results in a failure to respond to infection and disease. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Diagram of immune activation scale in the shape of a rainbow wedge, with 'vulnerable to infection' at the smaller end, 'sweet spot' in the middle, and 'autoimmunity' at the larger end" src="https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=260&fit=crop&dpr=1 600w, https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=260&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=260&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=326&fit=crop&dpr=1 754w, https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=326&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/559701/original/file-20231115-23-d6qlle.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=326&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Too much or too little immune activation can lead to illness.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Inflammation_scale.svg">Kevbonham/Wikimedia Commons</a>, <a class="license" href="http://creativecommons.org/licenses/by-sa/4.0/">CC BY-SA</a></span>
</figcaption>
</figure>
<p>Because sustaining <a href="https://www.nature.com/collections/mxwslsscsf">immune balance</a> is critical, tinkering with the immune system through the use of supplements is not a good idea unless you have a clinical deficiency in certain vital nutrients. For people with healthy levels of nutrients, taking supplements could lead to a false sense of security, particularly since the fine print on the back of supplements usually has <a href="https://www.fda.gov/food/information-consumers-using-dietary-supplements/questions-and-answers-dietary-supplements">this disclaimer</a> about their listed benefits: “This statement has not been evaluated by the FDA. Not intended to diagnose, treat, cure, or prevent any disease.”</p>
<p>Eating a <a href="https://www.hsph.harvard.edu/nutritionsource/nutrition-and-immunity/">well-balanced diet</a>, exercising regularly, reducing stress and getting decent sleep, on the other hand, can help your body maintain a functioning and healthy immune system. Although these lifestyle behaviors are not foolproof, they contribute to overall good health and ultimately to a more healthy immune system.</p>
<p>In reality, <a href="https://doi.org/10.1080/07853890.2017.1407035">vaccines are the only safe and effective tool</a> beyond healthy lifestyle behaviors to support your immune system. Vaccines contain harmless forms of pathogens that help to train your immune cells to recognize and fight them. When you come into contact with the real and harmful version of the pathogen out in the wild – whether it’s at a grocery store, social event or school – at a later date, these fully trained immune memory cells will immediately begin to fight and destroy the pathogen, sometimes so quickly that you don’t even realize you’ve been infected.</p>
<p>In a world where people are continually bombarded by the marketing mantra that more is better, rest assured that when it comes to the immune system, maintaining perfect balance is just right.</p><img src="https://counter.theconversation.com/content/215217/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Aimee Pugh Bernard is affiliated with Immunize Colorado and Colorado Immunization Advocates as an unpaid board member.</span></em></p>Dietary supplements claim to be able to ‘boost your immune system’ to combat disease. But attaining immune balance through a healthy lifestyle and vaccination is a safer bet to keep in good health.Aimee Pugh Bernard, Assistant Professor of Immunology and Microbiology, University of Colorado Anschutz Medical CampusLicensed 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/2134692023-09-21T04:22:22Z2023-09-21T04:22:22ZA COVID inquiry has been announced. But is COVID still a thing? Do I need a booster?<figure><img src="https://images.theconversation.com/files/549268/original/file-20230920-21-mzw4gi.jpg?ixlib=rb-1.1.0&rect=1%2C0%2C997%2C667&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/smiling-healthy-mature-older-senior-happy-2036186345">Shutterstock</a></span></figcaption></figure><p>Today’s <a href="https://www.abc.net.au/news/2023-09-21/inquiry-to-be-announced-into-aus-government-covid-19-response/102882616">announcement</a> <a href="https://www.pm.gov.au/media/improving-future-preparedness-inquiry-response-covid-19-pandemic">of an independent inquiry</a> into Australia’s COVID response will examine how we’ve handled the pandemic and how we could better prepare for the next one.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1704664168224444616"}"></div></p>
<p>But the pandemic is not just a once-in-a-lifetime event that’s over and needs to be analysed. It’s still with us.</p>
<p>The Omicron variant <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">continues to mutate</a> and <a href="https://www.abc.net.au/news/2023-09-21/new-covid-strain-variant-pirola-ba-2-86-in-australia-symptoms/102873304">new sub-variants</a> emerge. For instance, the highly-mutated BA.2.86 (known as Pirola) has just been <a href="https://www.abc.net.au/news/2023-09-21/new-covid-strain-variant-pirola-ba-2-86-in-australia-symptoms/102873304">detected</a> in Australia.</p>
<p>The SARS-CoV-2 virus, which causes COVID, then becomes more adept at evading immunity from infections and vaccines.</p>
<p>COVID is not yet predictably seasonal and we expect waves every three to six months. The United States has seen a <a href="https://covid.cdc.gov/covid-data-tracker/#trends_weeklyhospitaladmissions_select_00">threefold increase</a> in hospitalisations since mid-July due to waning immunity and the <a href="https://theconversation.com/the-who-has-declared-eris-a-variant-of-interest-how-is-it-different-from-other-omicron-variants-211276">EG.5 sub-variant</a> (known as Eris).</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/the-who-has-declared-eris-a-variant-of-interest-how-is-it-different-from-other-omicron-variants-211276">The WHO has declared Eris a 'variant of interest'. How is it different from other Omicron variants?</a>
</strong>
</em>
</p>
<hr>
<p>The United Kingdom has also seen a <a href="https://twitter.com/DrEricDing/status/1702790082749448202?t=FLc5f9FoMS6ksioFS8ATpA&s=09">significant increase</a> in adult and child hospitalisations due to COVID in the past month.</p>
<p>In Australia, more than <a href="https://www.worldometers.info/coronavirus/country/australia/">5,000 people</a> have died due to COVID so far this year. Excess deaths from any cause are <a href="https://www.abs.gov.au/statistics/health/causes-death/provisional-mortality-statistics/latest-release">13% higher</a> than expected. We expect many of these are related to COVID.</p>
<p>The median age of COVID deaths is <a href="https://www.abs.gov.au/articles/covid-19-mortality-australia-deaths-registered-until-31-july-2023">around 85 years old</a> in Australia. But there were 267 reported deaths in people under 50 until the end of July 2023; some may have had weaker immune systems. </p>
<p>The impacts of <a href="https://www.aph.gov.au/longandrepeatedcovid">long COVID and re-infections</a> are significant, which <a href="https://www.abc.net.au/news/2022-07-20/younger-active-female-data-reveals-long-covid-profile/101251352">one study shows</a> mainly affects people of working age and most commonly women.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/long-covid-symptoms-can-improve-but-their-resolution-is-slow-and-imperfect-212015">Long COVID symptoms can improve, but their resolution is slow and imperfect</a>
</strong>
</em>
</p>
<hr>
<h2>I’ve had a booster. Does that still protect me?</h2>
<p>We know immunity from COVID vaccines wanes over time. In a paper published in May, a <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2804451?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=050323">systematic review</a> of 40 studies showed by how much. Protection by the first two doses of the vaccine (known as the primary series) against symptomatic infection from Omicron waned from almost 53% one month after the second dose to just over 14% after six months.</p>
<p>The same review found a booster (third or fourth dose) increased protective immunity to the same levels as the primary series. However, that immunity waned to just 30% nine months later.</p>
<p>A number of studies have shown protection against severe disease and death from the Omicron variant also wanes over time. For example, <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(23)00365-1/fulltext#seccestitle10">a UK study</a> found a primary series plus a bivalent booster (targets two strains) provided 53% protection against hospitalisation four weeks after the booster among people aged 50 or over. Protection dropped to 36% at ten weeks.</p>
<p>An <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=4445191">Australian study</a>, yet to be independently verified by other researchers, suggests protection against death from COVID also wanes. Of 3.8 million adults over 65 years, protection of a third dose booster against death from COVID waned from an estimated 93% within three months to 56% after six months.</p>
<p>So we believe a reasonable interpetation of the above data is to recommend a booster every six months in people aged 75 and older, and younger people with impaired immune systems. </p>
<p>But in Australia, just over <a href="https://www.health.gov.au/sites/default/files/2023-09/covid-19-vaccine-rollout-update-15-september-2023.pdf">50%</a> of people aged 75 or older have received a booster in the past six months; only about 38% of people aged 65-74 and about 9% in those aged 18-64 years.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Older Asian couple happily walking along beach, looking at each other" src="https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=419&fit=crop&dpr=1 600w, https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=419&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=419&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=527&fit=crop&dpr=1 754w, https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=527&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/549274/original/file-20230920-29-ggj4d9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=527&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Just half of people aged 75 or older have received a booster in the past six months. Rates are even lower for people aged 65-74.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/happy-asian-seniors-walking-on-beach-156965456">Shutterstock</a></span>
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<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/over-half-of-eligible-aged-care-residents-are-yet-to-receive-their-covid-booster-and-winter-is-coming-205403">Over half of eligible aged care residents are yet to receive their COVID booster. And winter is coming</a>
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<hr>
<h2>I’ve had COVID recently. Surely that’s enough</h2>
<p>There is a widespread perception that if you’ve been infected with COVID and have had the primary series of the vaccine then you’re immune and, therefore, don’t need to get a booster. This is commonly described as having “hybrid immunity”. </p>
<p>However, a very <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)02465-5/fulltext">large study</a> across 19 countries found infection conferred different levels of immunity, depending on the variant. While infection with COVID effectively protected against reinfection by the original, Alpha, Beta and Delta variants, this was much less effective against the Omicron BA.1 variant. Since BA.1, there have been many new sub-variants that are even more adept at evading immunity.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1704601348073828483"}"></div></p>
<h2>Who can get a booster?</h2>
<p>Earlier this month, the Australian Technical Advisory Group on Immunisation (ATAGI) <a href="https://www.health.gov.au/news/atagi-update-on-the-covid-19-vaccination-program">recommended</a> all adults aged 75 or older “should receive” an additional dose of the bivalent vaccine if six months have passed since their last dose. Additionally, people aged 65-74 and immunocompromised younger adults should “consider” an additional dose.</p>
<p>ATAGI argues that the baseline risk of severe illness in people under 65 is low if they have already been vaccinated, and particularly if they have also been infected. So, a further 2023 dose for this group would offer little additional benefit, even if it has been more than six months since their last dose.</p>
<p>The US has taken a different approach. Last week, the Centers for Disease Control and Prevention <a href="https://www.cdc.gov/media/releases/2023/p0912-COVID-19-Vaccine.html">recommended</a> all people over six months who have not received a COVID vaccine in the previous two months should get a dose of the newly approved monovalent (single strain) vaccines. These have been developed by Pfizer and Moderna to specifically <a href="https://www.fda.gov/news-events/press-announcements/fda-takes-action-updated-mrna-covid-19-vaccines-better-protect-against-currently-circulating">target the XBB.1.5</a> sub-variant of Omicron. <a href="https://www.canada.ca/en/health-canada/news/2023/09/health-canada-authorizes-moderna-covid-19-vaccine-targeting-the-omicron-xbb15-subvariant.html">Health Canada</a> has adopted similar recommendations.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1701718604373229991"}"></div></p>
<p>These new monovalent vaccines are expected <a href="https://www.science.org/content/article/should-i-get-covid-19-booster">to be effective</a> in preventing infection by recently emerging Omicron sub-variants, such as EG.5 and FL.1.51 derived from the XBB.1.5 sub-variant, and the newer highly mutated <a href="https://www.gov.uk/government/publications/investigation-of-sars-cov-2-variants-of-concern-variant-risk-assessments/risk-assessment-for-sars-cov-2-variant-v-23aug-01-or-ba286">BA.2.86</a>, which arose from an earlier sub-variant and is a significant evolutionary leap.</p>
<p>While Canada and the US move into the northern hemisphere winter, Australians should not believe they are at lower risk during the summer. After all, <a href="https://www.worldometers.info/coronavirus/country/australia/">two large COVID waves</a> in Australia were in the summers of 2021/22 and 2022/23.</p>
<p>Monovalent XBB.1.5 vaccines are not yet available in Australia, but are being evaluated by the <a href="https://www.tga.gov.au/products/covid-19/covid-19-vaccines/covid-19-vaccines-regulatory-status">Therapeutic Goods Administration</a>. So, in the future, Australia’s advice about who’s eligible for a booster, and which type of booster, may change.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/cdc-greenlights-two-updated-covid-19-vaccines-but-how-will-they-fare-against-the-latest-variants-5-questions-answered-213341">CDC greenlights two updated COVID-19 vaccines, but how will they fare against the latest variants? 5 questions answered</a>
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</em>
</p>
<hr>
<h2>So, how do I decide if I need a booster now?</h2>
<p>There is evidence in Australia of <a href="https://www.abc.net.au/news/2023-09-21/new-covid-strain-variant-pirola-ba-2-86-in-australia-symptoms/102873304">growth of</a> the newer subvariants, including the detection of BA.2.86. So all Australians aged 75 and over who have not had a booster in the past six months should immediately have the currently available bivalent vaccine.</p>
<p>Younger age groups may wait until further ATAGI advice about the new monovalent vaccines.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1698591923781484711"}"></div></p>
<h2>COVID is not over</h2>
<p>While there is no need for alarm, Australians need to be aware of the ongoing significant impacts of COVID. The SARS-CoV-2 virus is still a formidable foe as it continues to mutate.</p>
<p>COVID vaccines will be <a href="https://www.pm.gov.au/media/improving-future-preparedness-inquiry-response-covid-19-pandemic">among the topics</a> the newly announced inquiry will investigate.</p>
<p>But we cannot rely on vaccines alone. Avoiding (re)infection is also vital. Breathe <a href="https://www.coronavirus.vic.gov.au/ventilation">clean indoor air</a>, wear <a href="https://www.cdc.gov/coronavirus/2019-ncov/prevent-getting-sick/types-of-masks.html">high quality masks</a> and get tested so you can access <a href="https://www.health.gov.au/health-alerts/covid-19/treatments/eligibility">antivirals</a> if eligible.</p><img src="https://counter.theconversation.com/content/213469/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Michael Toole receives funding from the National Health and Medical Research Council.</span></em></p><p class="fine-print"><em><span>Heidi Drummer has acted as a consultant for Moderna. Heidi Drummer receives funding from the Medical Research Future Fund and mRNA Victoria and is President of the Australasian Virology Society.</span></em></p><p class="fine-print"><em><span>Suman Majumdar, through the Burnet Institute receives grant funding from the Australian governemnt via the National Health & Medical Research Council of Australia, the Medical Research Future Fund and DFAT's Centre for Health Security.
</span></em></p>Australia seems to be focusing on boosters for people aged 75 and over, with its latest recommendations. But that may change.Michael Toole, Associate Principal Research Fellow, Burnet InstituteHeidi Drummer, Professor and Co-Program Director, Disease Elimination, Burnet InstituteSuman Majumdar, Associate Professor and Chief Health Officer - COVID and Health Emergencies, Burnet InstituteLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2105652023-08-24T20:20:43Z2023-08-24T20:20:43ZWhy do I crave sugar and carbs when I’m sick?<figure><img src="https://images.theconversation.com/files/544126/original/file-20230823-24-jor56l.jpg?ixlib=rb-1.1.0&rect=0%2C179%2C5991%2C3808&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://unsplash.com/photos/imAfCYq7KH0">Adrian Swancar/Unsplash</a></span></figcaption></figure><p>Your nose is running, your head hurts and you feel like you’re coming down with a cold. You’re settling in on the couch for a sick day. Then you reach for the snacks. </p>
<p>When you’re sick, your appetite often decreases. So why, at other times, do you crave sugary treats and carbohydrate-loaded comfort foods?</p>
<p>A food <a href="https://pubmed.ncbi.nlm.nih.gov/28375878/">craving</a> goes beyond a mere desire to eat, it encompasses a <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399671/#CR1">complex mix</a> of emotional, behavioural, cognitive and physiological processes. Whether it’s the need for a quick energy source or a temporary relief from discomfort, our bodies and minds work in tandem to drive our food preferences.</p>
<p>Here we’ll explore the science behind why our bodies crave sugar and carbs – especially when we’re sick.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/3-reasons-you-feel-hungrier-and-crave-comfort-foods-when-the-weather-turns-cold-202831">3 reasons you feel hungrier and crave comfort foods when the weather turns cold</a>
</strong>
</em>
</p>
<hr>
<h2>Fuelling the immune system</h2>
<p>When sickness strikes, our immune system springs into action, requiring additional energy to combat invaders. </p>
<p>This heightened activity often leads to an increase in our <a href="https://pubmed.ncbi.nlm.nih.gov/36505552/">metabolic rate</a>, energy demands and nutritional requirements. </p>
<p>Sugary treats and carbs are quick sources of energy, satisfying this increased demand. </p>
<figure class="align-center ">
<img alt="Person eats a biscuit" src="https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544124/original/file-20230823-5286-u508sw.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">Sugary treats are a quick source of energy.</span>
<span class="attribution"><a class="source" href="https://www.pexels.com/photo/person-holding-biscuit-with-both-hands-1204222/">Cats coming/Pexels</a></span>
</figcaption>
</figure>
<p>But while a high sugar diet during times of illness may help meet increased metabolic demands, it could also exacerbate the immune and inflammatory response, potentially impeding recovery. </p>
<p>In the longer term, high-sugar diets promote chronic <a href="https://pubmed.ncbi.nlm.nih.gov/33339337/">inflammation</a>, <a href="https://www.science.org/doi/10.1126/scitranslmed.aay6218?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">alter gut microbiota</a> composition, and are associated with chronic disease. For a <a href="https://www.mdpi.com/2072-6643/12/4/1181">well-functioning immune system</a>, aim for a <a href="https://www.who.int/news-room/fact-sheets/detail/healthy-diet">balanced intake</a> of <a href="https://pubmed.ncbi.nlm.nih.gov/31267783/">fruits, vegetables</a>, fibre, protein, and low-glycaemic carbohydrates.</p>
<h2>The stress response</h2>
<p>Being sick is stressful for the body. Acute mild or intense stress, like we’d see if we’re sick, boosts the “<a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5921333/">flight or fight</a>” hormones adrenaline and cortisol. This mobilises stored energy to meet increased demands, but it can also curb appetite. </p>
<p><a href="https://pubmed.ncbi.nlm.nih.gov/31125634/">Prolonged stress</a> can disrupt energy balance, and cause nutritional deficiencies and alterations in gut and brain functions. This can reduce a person’s threshold for craving sugar and salt, increasing their preferences towards energy-dense foods.</p>
<p>The stress hormone cortisol can also increase your <a href="https://pubmed.ncbi.nlm.nih.gov/24123563/">preference</a> for high-calorie, comfort foods, which can <a href="https://pubmed.ncbi.nlm.nih.gov/36615866/">temporarily alleviate stress</a>. </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>
<h2>The brain’s reward system</h2>
<p>Comfort foods trigger your brain’s reward system, releasing feel-good neurotransmitters like <a href="https://pubmed.ncbi.nlm.nih.gov/30595479/">dopamine</a> and serotonin. </p>
<p>But “<a href="https://pubmed.ncbi.nlm.nih.gov/30951762/">sugar rushes</a>” are often short-lived and can lead to decreased alertness and heightened fatigue within an hour of consumption. </p>
<p>The link between carbohydrates (which the body converts to sugar) and serotonin can be traced back to 1971 when <a href="https://www.science.org/doi/10.1126/science.174.4013.1023?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">researchers</a> found elevated tryptophan levels (serotonin’s precursor) in rats’ plasma and brains after a carbohydrate-rich diet. </p>
<p>Subsequent studies in humans established connections between carbohydrates and mood, especially in relation to <a href="https://pubmed.ncbi.nlm.nih.gov/2903717/">obesity, depression and seasonal affective disorder</a>. Therapies enhancing serotonin have since been shown to <a href="https://pubmed.ncbi.nlm.nih.gov/2903717/">reduce carbohydrate intake</a>.</p>
<figure class="align-center ">
<img alt="McDonald's French fries" src="https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=450&fit=crop&dpr=1 600w, https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=450&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=450&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=566&fit=crop&dpr=1 754w, https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=566&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/544140/original/file-20230823-27-lqld1n.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">There’s more to our cravings than just a desire to eat.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/MyuR5q3KDmw">Unsplash/Brett Jordan</a></span>
</figcaption>
</figure>
<p>Remarkably, around <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8911970/pdf/molecules-27-01680.pdf">90% of serotonin</a> production occurs in the gut. The vast microbial population in our gut exerts a potent influence on <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8106557/">immunity, metabolism</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8293578/pdf/40168_2021_Article_1093.pdf">appetite</a>. </p>
<p>Recent mouse studies have even identified specific microbes linked to <a href="https://www.cell.com/current-biology/fulltext/S0960-9822(22)01750-X">sugar binges after antibiotic treatment</a>.</p>
<h2>Some people eat less when they’re sick</h2>
<p>Not everyone craves sugar and carbs when they are sick. Some people eat less for a few reasons:</p>
<ul>
<li><p>they have less of an appetite. While <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5610818/pdf/JDR2017-4527980.pdf">ghrelin</a> (the “hunger” hormone) levels might initially rise, prolonged illness can suppress appetite due to nausea, fatigue and discomfort. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5921333/">Critically ill</a> patients have reduced food intake and are at risk of malnutrition</p></li>
<li><p><a href="https://pubmed.ncbi.nlm.nih.gov/30777142/">metabolic adaptation</a>. The body might slow specific metabolic processes to conserve energy, reducing overall calorie requirements</p></li>
<li><p>altered taste perception. <a href="https://pubmed.ncbi.nlm.nih.gov/32195512/#:%7E:text=The%20ability%20of%20an%20individual%20to%20perceive%20tastes,intake%2C%20playing%20an%20important%20role%20in%20promoting%20satiation%2Fsatiety.">Taste</a> is an important component that affects both appetite and energy intake. Alterations in taste and smell is a common symptom when we are sick and was common with <a href="https://doi.org/10.1101/2020.04.05.20048421">COVID</a></p></li>
<li><p>consuming fluids like water, tea or broths might be more appealing and manageable than solid foods. These fluids provide hydration but contribute minimally to calorie intake.</p></li>
</ul>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/what-to-eat-when-you-have-covid-and-why-reaching-for-the-chicken-soup-is-not-a-bad-idea-202338">What to eat when you have COVID – and why reaching for the chicken soup is not a bad idea</a>
</strong>
</em>
</p>
<hr>
<img src="https://counter.theconversation.com/content/210565/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Hayley O'Neill is a wellness coach for Hayley M O'Neill Enterprises.</span></em></p>A quick energy source or a temporary relief from discomfort? Here’s what drives our food preferences when we’re sick.Hayley O'Neill, Assistant Professor, Faculty of Health Sciences and Medicine, Bond UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2088022023-08-17T10:50:21Z2023-08-17T10:50:21ZHow biological differences between men and women alter immune responses – and affect women’s health<figure><img src="https://images.theconversation.com/files/539557/original/file-20230726-21-jhiwex.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C3849%2C2568&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/wooden-cubes-image-male-female-gender-2175270281">Fida Olga/Shutterstock</a></span></figcaption></figure><p>Most people will have heard the term “man flu”, which refers to men’s perceived tendency to exaggerate the severity of a cold or a similar minor ailment. </p>
<p>What most people may not know is that, generally speaking, women mount stronger <a href="https://pubmed.ncbi.nlm.nih.gov/36121220/">immune responses</a> to infections than men. Men are <a href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005374">more susceptible</a> to infections from, for example, HIV, hepatitis B, and <em>Plasmodium falciparum</em> (the parasite responsible for malaria). </p>
<p>They can also have more severe symptoms, with evidence showing they’re more likely to be <a href="https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1005374">admitted to hospital</a> when infected with hepatitis B, tuberculosis, and <em>Campylobacter jejuni</em> (a bacteria that causes gastroenteritis), among others.</p>
<p>While this may be positive for women in some respects, it also means women are at <a href="https://www.nature.com/articles/nri2815">greater risk</a> of developing chronic diseases driven by the immune system, known as immune-mediated inflammatory diseases.</p>
<hr>
<figure class="align-right ">
<img alt="" src="https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/542294/original/file-20230811-4652-hn8w80.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">
<figcaption>
<span class="caption"></span>
</figcaption>
</figure>
<p><em>This article is part of <a href="https://theconversation.com/uk/topics/womens-health-matters-143335">Women’s Health Matters</a>, a series about the health and wellbeing of women and girls around the world. From menopause to miscarriage, pleasure to pain the articles in this series will delve into the full spectrum of women’s health issues to provide valuable information, insights and resources for women of all ages.</em></p>
<p><em>You may be interested in:</em></p>
<p><em><a href="https://theconversation.com/the-orgasm-gap-and-why-women-climax-less-than-men-208614">The orgasm gap and why women climax less than men</a></em></p>
<p><em><a href="https://theconversation.com/five-old-contraception-methods-that-show-why-the-pill-was-a-medical-breakthrough-207572">Five old contraception methods that show why the pill was a medical breakthrough
</a></em></p>
<p><em><a href="https://theconversation.com/science-experiments-traditionally-only-used-male-mice-heres-why-thats-a-problem-for-womens-health-205963">Science experiments traditionally only used male mice – here’s why that’s a problem for women’s health</a></em></p>
<hr>
<p>Here we will explore how biological factors influence immune differences between the sexes and how this affects women’s health. While we acknowledge that both sex and gender may affect immune responses, this article will focus on biological sex rather than gender. </p>
<h2>Battle of the sexes</h2>
<p>There are differences <a href="https://www.nature.com/articles/nri.2016.90">between the sexes</a> at every stage of the immune response, from the number of immune cells, to their degree of activation (how ready they are to respond to a challenge), and beyond.</p>
<p>However, the story is more complicated than that. Our immune system evolves throughout our lives, learning from past experiences, but also responding to the physiological challenges of getting older. As a result, <a href="https://www.nature.com/articles/nri.2016.90">sex differences</a> in the immune system can be seen from birth through puberty into adulthood and <a href="https://academic.oup.com/jleukbio/advance-article/doi/10.1093/jleuko/qiad053/7190870">old age</a>.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/discovery-of-gene-associated-with-20-autoimmune-diseases-leads-to-promising-drug-trials-131957">Discovery of gene associated with 20 autoimmune diseases leads to promising drug trials</a>
</strong>
</em>
</p>
<hr>
<p>Why do these differences occur? The first part of answering this question involves the X chromosome. Females have two X chromosomes, while males have one X and one Y chromosome. The <a href="https://pubmed.ncbi.nlm.nih.gov/20651746/">X chromosome</a> contains the largest number of immune-related genes. </p>
<p>The X chromosome also has <a href="https://link.springer.com/article/10.1007/s00018-020-03526-7">around 118 genes</a> from a gene family that are able to stop the expression of other genes, or change how proteins are made, including those required for immunity. These gene-protein regulators are known as microRNA, and there are only <a href="https://pubmed.ncbi.nlm.nih.gov/24808907/">two microRNA genes</a> on the Y chromosome.</p>
<p>The X chromosome has <a href="https://www.genome.gov/about-genomics/fact-sheets/X-Chromosome-facts">more genes overall</a> (around 900) than the Y chromosome (around 55), so female cells have evolved to switch off one of their X chromosomes. This is not like turning off a light switch, but more like using a dimmer. </p>
<p>Around <a href="https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-019-5507-6">15-25% of genes</a> on the silenced X chromosome are expressed at any given moment in any given cell. This means female cells can often express more immune-related genes and gene-protein regulators than males. This generally means a faster clearance of pathogens in females than males.</p>
<figure class="align-center ">
<img alt="Three women laughing together outdoors." src="https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539933/original/file-20230728-19-fesqbz.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">Women have two X chromosomes, which partly explains why the female immune system works differently.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/mature-female-friends-socializing-backyard-together-583329838">Monkey Business Images/Shutterstock</a></span>
</figcaption>
</figure>
<p>Second, men and women have <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2020.604000/full">varying levels</a> of different sex hormones. Progesterone and testosterone are broadly considered to limit immune responses. While both hormones are produced by males and females, progesterone is found at higher concentrations in non-menopausal women than men, and testosterone is much higher in men than women. </p>
<p>The role of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6533072/">oestrogen</a>, one of the main female sex hormones, is more complicated. Although generally oestrogen <a href="https://www.sciencedirect.com/science/article/abs/pii/S000887491500026X?via%3Dihub">enhances immune responses</a>, its levels vary during the menstrual cycle, are high in pregnancy and low after menopause. </p>
<p>Due in part to these genetic and hormonal factors, pregnancy and the years following are associated with heightened immune responses to external challenges such as infection. </p>
<p>This has been regarded as an <a href="https://www.nature.com/articles/nri.2016.90">evolutionary feature</a>, protecting women and their unborn children during pregnancy and enhancing the mother’s survival throughout the child-rearing years, ultimately ensuring the survival of the population. We also see this pattern in <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2628977/">other species</a> including insects, lizards, birds and mammals. </p>
<h2>What does this all mean?</h2>
<p>With women’s heightened immune responses to infections comes an increased risk of certain diseases and prolonged immune responses after infections.</p>
<p>An <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3328995/">estimated 75-80%</a> of all immune-mediated inflammatory diseases <a href="https://pubmed.ncbi.nlm.nih.gov/32542149/">occur in females</a>. Diseases more common in women include multiple sclerosis, <a href="https://www.nature.com/articles/nri2815">rheumatoid arthritis</a>, lupus, Sjogren’s syndrome, and <a href="https://www.nature.com/articles/nri.2016.90">thyroid disorders</a> such as Graves disease.</p>
<p>In these diseases, the immune system is continuously fighting against what it sees as a foreign agent. However, often this perceived threat is not a foreign agent, but cells or tissues from the host. This leads to tissue damage, pain and immobility.</p>
<p>Women are also prone to chronic inflammation following infection. For example, after infections with <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5818468/">Epstein Barr virus</a> or <a href="https://www.liebertpub.com/doi/10.1089/jwh.2008.1193">Lyme disease</a>, they may go on to develop <a href="https://www.nhs.uk/conditions/chronic-fatigue-syndrome-cfs/">chronic fatigue syndrome</a>, another condition that affects more women than men.</p>
<p>This is one possible explanation for the heightened risk among <a href="https://www.frontiersin.org/articles/10.3389/fresc.2023.1122673/full">pre-menopausal women</a> of developing long COVID following infection with SARS-CoV-2, the virus that causes COVID. </p>
<p>Research has also revealed the presence of auto-antibodies (antibodies that attack the host) in patients with long COVID, suggesting it might be an <a href="https://www.sciencedirect.com/science/article/pii/S1568997221000550">autoimmune disease</a>. As women are more susceptible to autoimmune conditions, this could potentially explain the sex bias seen. </p>
<p>However, the exact causes of long COVID, and the reason women may be at greater risk, are yet to be defined. </p>
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<strong>
Read more:
<a href="https://theconversation.com/long-covid-female-sex-older-age-and-existing-health-problems-increase-risk-new-research-185911">Long COVID: female sex, older age and existing health problems increase risk – new research</a>
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<p>This paints a bleak picture, but it’s not all bad news. Women typically mount <a href="https://pubmed.ncbi.nlm.nih.gov/24966191/">better vaccine responses</a> to several common infections (for example, influenza, measles, mumps, rubella, hepatitis A and B), producing higher antibody levels than men. </p>
<p>One study showed that women vaccinated with half a dose of flu vaccine produced the same amount of antibodies compared to men vaccinated with <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/773453">a full dose</a>. </p>
<p>However, these responses <a href="https://www.nature.com/articles/nri.2016.90">decline as women age</a>, and particularly <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3954964/">after menopause</a>. </p>
<p>All of this shows it’s vital to consider sex when designing studies examining the immune system and treating patients with immune-related diseases.</p><img src="https://counter.theconversation.com/content/208802/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Helen McGettrick receives funding from the Medical Research Council, Biotechnology and Biological Sciences Research Council, Wellcome Trust, F Hoffmann-La Roche Ag, Versus Arthritis, Dompè Pharmaceuticals Ltd, Novartis, Chernajovsky Foundation, British Heart Foundation, Pfizer. </span></em></p><p class="fine-print"><em><span>Asif Iqbal receives funding from, Wellcome Trust, F Hoffmann-La Roche, Chernajovsky Foundation, British Heart Foundation. </span></em></p>Women are more likely to develop chronic diseases driven by the immune system.Helen McGettrick, Reader in Inflammation and Vascular Biology, University of BirminghamAsif Iqbal, Associate Professor in Inflammation Biology, University of BirminghamLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2110192023-08-07T14:04:16Z2023-08-07T14:04:16ZCOVID: here’s why cases have seen a small spike this summer<figure><img src="https://images.theconversation.com/files/541463/original/file-20230807-24547-eqraxl.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C4666%2C3101&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Summer travel may partly be spurring the spike.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/naples-italy-august-2019-people-queuing-1601789095">Ceri Breeze/ Shutterstock</a></span></figcaption></figure><p>Since the beginning of July all there have been indications that COVID infections are increasing again in the UK.</p>
<p>The daily number of <a href="https://coronavirus.data.gov.uk/details/cases?areaType=nation&areaName=England">new positive tests</a> and the proportion of tests <a href="https://coronavirus.data.gov.uk/details/testing?areaType=nation&areaName=England">coming back positive</a> have been increasing since the end of June. New admissions to hospital with COVID and the number of beds occupied by COVID patients <a href="https://coronavirus.data.gov.uk/details/healthcare?areaType=nation&areaName=England">have also increased</a> compared to levels seen at the end of June. </p>
<p>The latest official government data suggests that <a href="https://coronavirus.data.gov.uk/details/cases?areaType=nation&areaName=England">infections and hospitalisations are still rising</a>. On the other hand, the Zoe App data (which is used to track COVID symptoms and infections) suggests that the current wave <a href="https://storage.cloud.google.com/covid-public-data/report/zoe_health_study_report_20230802.pdf?_ga=2.59582376.-446265578.1691072229">may have already peaked</a>. </p>
<p>But with the Office for National Statistics no longer publishing <a href="https://theconversation.com/the-ons-has-published-its-final-covid-infection-survey-heres-why-its-been-such-a-valuable-resource-20258">COVID infection data</a>, it’s not now possible to know with any degree of certainty just how many infections are actually happening in the UK each day – only how many tests have come back positive. But even with the July spike in infections and hospital admissions, hospital cases are still far lower than the levels we saw in previous summers – and even earlier this year. </p>
<p>There are a couple of reasons why there’s been a spike in COVID cases in the UK this summer. While part of it comes down to a new variant and foreign travel over the summer holidays, the increase in cases may also be a sign that COVID is now endemic in the population.</p>
<h2>Why cases have spiked</h2>
<p>Most infectious disease scientists and specialists have known since very early in the pandemic that <a href="https://www.nature.com/articles/d41586-021-00396-2">eradicating the virus</a> was unachievable, and that eventually COVID would become endemic – just as the common cold and flu are. </p>
<p>Evidence since then has confirmed that immunity against infection, either from immunisation or following infection, is <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(22)00801-5/fulltext">very short-lived</a> – only a matter of a few months. Even people with so-called hybrid immunity (those who have been immunised and had an infection) do not have protection against reinfection for much longer.</p>
<p>With such short protection against infection, we can calculate then – based on the duration of immunity and a person’s susceptibility to infection – that as COVID heads towards being endemic it will likely still cause an average of <a href="https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(21)00219-6/fulltext">around 80,000</a> new infections each day in England for years to come. </p>
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<em>
<strong>
Read more:
<a href="https://theconversation.com/how-will-the-covid-pandemic-end-167244">How will the COVID pandemic end?</a>
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<p>Epidemic models that account for short-lasting immunity also predict that as an epidemic heads toward being endemic, it does so in a series of <a href="https://www.nature.com/articles/s41592-020-0856-2">increasingly dampened waves</a>. And, as an infection approaches being endemic, the impact of interventions aimed at reducing transmission such as social distancing and face coverings have much less affect on infection numbers than they did earlier in the pandemic. This is because infection rates in the population are then driven mainly by the <a href="https://www.nature.com/articles/s41592-020-0856-2">rate at which immunity is lost</a>. </p>
<figure class="align-center ">
<img alt="A young man receives a jab from a doctor or nurse." src="https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/541464/original/file-20230807-26-4exzf6.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">Immunity against COVID, even after a vaccine, only lasts a few months.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/close-unrecognizable-male-nurse-injecting-vaccine-1891457239">SeventyFour/ Shutterstock</a></span>
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<p>So, the current increase in infections should not come as any surprise, nor is it anything to be too concerned about. </p>
<p>Since the omicron variant became dominant in December 2021, we have been seeing waves in reported infections about every three months, which is similar to the rate at which <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(22)00801-5/fulltext">immunity is lost</a> following vaccination. But each subsequent wave after omicron has generally seen fewer people in hospital. So each wave has, so far, caused less severe disease than the previous peaks. </p>
<p>Although this latest increase would likely to have happened anyway, there may be some additional push from the start of the holiday season. For instance, foreign travel post-omicron was a significant <a href="https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/coronaviruscovid19infectionsurveycharacteristicsofpeopletestingpositiveforcovid19uk/25may2022">risk factor for infection</a> in the UK in early 2022. How much of this association of COVID risk with international travel was due to infection in airports, during travel or socialising while overseas is unclear and whether international travel is still a risk factor is not certain – but in my opinion it probably is.</p>
<p>There’s also a new variant, called EG.1.5, which is now responsible for about <a href="https://cov-spectrum.org/explore/United%20Kingdom/AllSamples/Past6M/variants?nextcladePangoLineage=EG.5.1*&">15% of infections in the UK</a>. But while this new variant only makes up a small proportion of current COVID cases, infections from this new variant are on the rise. This is because mutations on the virus reduce the immune system’s ability to prevent an infection – even in people who have immunity to other variants.</p>
<h2>Looking forward</h2>
<p>In previous years we’ve seen increases in total infections around the time that schools <a href="https://www.ons.gov.uk/file?uri=/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/datasets/coronaviruscovid19infectionsurveyheadlineresultsuk/2023/previous/v1/20230217headlinedataset.xlsx">returned from the summer break</a>. But it’s uncertain how much transmission in schools actually contribute to these spikes – or whether it was due to other factors, such as returning from travelling abroad.</p>
<p>In the longer term, we will continue to see waves of COVID infections for years. Given what we know about <a href="https://academic.oup.com/jid/article/222/1/9/5815743">other human coronavirus infections</a>, we’ll probably see COVID settle into a seasonal pattern – with infections peaking each year sometime between November and February. Such seasonality is seen in most respiratory viral infections. Though the reasons for this are still <a href="https://www.clinicalmicrobiologyandinfection.com/article/S1198-743X(14)61091-0/fulltext">not fully understood</a>, it could be due to more time spent indoors close to other people, lowered immunity in the winter months and viruses being better able to survive in colder weather.</p>
<p>Despite increased infections in winter being the norm, this current summer wave was expected and is not something we should be overly concerned about. We will continue to see future waves of COVID infections. </p>
<p>The number of severe COVID infections will also probably continue to fall over the next few years, <a href="https://www.england.nhs.uk/statistics/statistical-work-areas/covid-19-hospital-activity/">as has already been happening</a>. In fact, many infectious disease scientists believed back in 2020 that SARS-CoV-2 will eventually become <a href="https://www.nature.com/articles/d41586-021-00396-2">just another cause of the common cold</a>. </p>
<p>But if you are vulnerable to severe COVID and want to protect yourself, it’s important to always accept vaccine boosters when offered. Wear face coverings may also <a href="https://link.springer.com/article/10.1007/s11606-020-06067-8">reduce the severity of illness</a> following infection.</p><img src="https://counter.theconversation.com/content/211019/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Paul Hunter consults for the World Health Organization. He receives funding from National Institute for Health Research, the World Health Organization and the European Regional Development Fund.</span></em></p>The current increase in infections is not any surprise to disease scientists – nor is it anything to be too concerned about.Paul Hunter, Professor of Medicine, University of East AngliaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2093342023-08-03T00:37:55Z2023-08-03T00:37:55ZWhat are lymph nodes? And can a massage really improve lymphatic drainage?<figure><img src="https://images.theconversation.com/files/539191/original/file-20230725-18-nxo5lk.jpg?ixlib=rb-1.1.0&rect=93%2C17%2C3789%2C2566&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/lymphatic-drainage-massage-legs-lower-female-1787444039">Shutterstock</a></span></figcaption></figure><p>The lymphatic system has long been considered mysterious. </p>
<p>Unlike blood vessels, lymphatic vessels are not very visible to the naked eye, even during surgery. Because of this, the anatomy and functions of the lymphatic system have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312397/">historically</a> not been well studied. The fluid in the lymphatic system was <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554832/">named</a> “lymph” after the Greek <em>nymph</em> – a mythical creature associated with clear streams – and the Roman <em>Lympha</em>, goddesses of fresh water.</p>
<p>But the lymphatic system – and the lymph nodes within it – plays fascinating and <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/joa.12644">important roles</a> in health and disease, from fighting off infection to maintain the body’s fluid balance.</p>
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<strong>
Read more:
<a href="https://theconversation.com/what-can-go-wrong-in-the-blood-a-brief-overview-of-bleeding-clotting-and-cancer-76400">What can go wrong in the blood? A brief overview of bleeding, clotting and cancer</a>
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<h2>A major part of our immune system</h2>
<p>The lymphatic system protects the body against foreign invaders and enables us to mount an immune response. </p>
<p><a href="https://www.genome.gov/genetics-glossary/Lymphocyte#:%7E:text=A%20lymphocyte%20is%20a%20type,bacteria%2C%20viruses%2C%20and%20toxins">Lymphocytes</a> are the cells of the lymphatic system. These are a type of white blood cell and include B cells and T cells. B cells produce antibodies to attack invading pathogens such as bacteria and viruses. T cells destroy the body’s own cells if they become cancerous or infected.</p>
<p>Lymphocytes are mostly contained in about 700 peanut-sized lymph glands in the body. Enlarged lymph nodes, such as <a href="https://theconversation.com/covid-vaccine-may-lead-to-a-harmless-lump-in-your-armpit-so-women-advised-to-delay-mammograms-for-6-weeks-159529">after a vaccination</a> or with an infection, are due to lymphocytes mounting a protective immune response. <a href="https://www.mayoclinic.org/diseases-conditions/lymphoma/symptoms-causes/syc-20352638">Lymphoma</a> is a cancer that happens when lymphocytes multiply uncontrollably and cause swollen lymph glands throughout the body. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="diagram of human torso with green lines showing lymph nodes and vessels" src="https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539188/original/file-20230725-15-28tkq.jpg?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"></a>
<figcaption>
<span class="caption">There are around 700 lymph nodes around the body.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/lymphatic-system-internal-anatomy-male-chest-1429903247">Shutterstock</a></span>
</figcaption>
</figure>
<p>We also have lymphatic tissue in parts our airways and digestive system because these areas are exposed to external bugs via the air we breath or the things we eat and drink. In the digestive system, the lymphatic system also has an <a href="https://www.frontiersin.org/articles/10.3389/fphys.2022.846936/full">essential role</a> in absorbing dietary fat from the intestines.</p>
<p>Some lymphocytes <a href="https://www.ncbi.nlm.nih.gov/books/NBK26921/#:%7E:text=The%20answer%20is%20that%20they,small%20veins%20called%20postcapillary%20venules">travel around the body</a> conducting pathogen surveillance for invading bugs. They circulate between lymph nodes, lymph and the blood. </p>
<h2>A fine balance of fluids</h2>
<p>Every day, about <a href="https://bio.libretexts.org/Courses/Lumen_Learning/Biology_of_Aging_(Lumen)/10%3A_The_Immune_System/10.01%3A_Anatomy_of_the_Lymphatic_and_Immune_Systems">20 litres</a> of fluid is pushed out of capillaries – our smallest blood vessels – into tissues and organs. This is driven by blood pressure and is how tissues get oxygen and energy. About 17 litres of this fluid returns to the veins, alongside carbon dioxide and other waste products.</p>
<p>But what happens to the remaining 3 litres of fluid? </p>
<p>If it stayed in our tissues, it would cause swelling called <a href="https://www.ncbi.nlm.nih.gov/books/NBK482447/">oedema</a>, sometimes referred to as fluid retention.</p>
<p>Luckily, our lymphatic vessels usually pick up this remaining 3 litres of fluid and <a href="https://pubmed.ncbi.nlm.nih.gov/17901744/">return it</a> to the blood circulation. </p>
<p>Starting in the tissues just under the skin and around our organs, the lymphatic system is a one-way circulatory system. Lymphatic vessels carry lymph from the tissues via lymph nodes and then into veins that drain directly into the heart. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="woman takes deep breaths outside. Hand on chest" src="https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=429&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=429&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=429&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=539&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=539&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539196/original/file-20230725-15-6avf8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=539&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Deep breathing can help lymphatic flow.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-mutliethnic-woman-practices-deep-belly-2293569205">Shutterstock</a></span>
</figcaption>
</figure>
<h2>A slow flow</h2>
<p>Unlike the blood circulation, the lymphatic circulation is <a href="https://www.britannica.com/science/lymph">not driven</a> by the pumping of the heart. Lymph is moved towards the heart by muscular contractions of the lymphatic vessels and one-way valves.</p>
<p>Movement, exercise and deep breathing all help to move lymph through lymphatic vessels. </p>
<p>It is difficult to move lymph against gravity, and lymph can <a href="https://my.clevelandclinic.org/health/diseases/12564-edema">accumulate</a> and cause swelling or oedema in the legs and feet. Many people have experienced this as swollen feet after standing still for too long or sitting during a long-haul flight. </p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="grey scale drawn diagram of upper body from back view" src="https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=819&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=819&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=819&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1029&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1029&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539185/original/file-20230725-21-mqxwrk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1029&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Paolo Mascagni’s 1787 diagram of the upper body’s lymphatic system.</span>
<span class="attribution"><a class="source" href="https://wellcomecollection.org/works/mgvcasb3">Wellcome Collection</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<h2>Too much fluid</h2>
<p>Oedema can also occur when too much fluid moves out of the capillaries and overloads the capacity of the lymphatic vessels to reabsorb it. </p>
<p>This can be due to heart failure, chronic venous insufficiency, liver failure or kidney disease. In our research, we found 49% of people with chronic venous insufficiency (or poor blood flow in the veins) had <a href="https://www.sciencedirect.com/science/article/abs/pii/S2213333X20301104">leg oedema</a>.</p>
<p><a href="https://pubmed.ncbi.nlm.nih.gov/17901744/#:%7E:text=Physical%20examination%20should%20focus%20on,modalities%2C%20including%20CT%20or%20MRI">Lymphoedema</a> is when the oedema is caused by a problem with the lymphatic system. This is commonly due to obstruction of lymph drainage or removal of lymph nodes during cancer treatment. </p>
<h2>Treatments can help lymph flow more freely</h2>
<p>Lymphoedema <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5508242/">treatments</a> include lymphatic massage, compression bandages or stockings, and exercise. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Person sits on bed and pulls on compression bandage. Ankles are swollen" src="https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=369&fit=crop&dpr=1 600w, https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=369&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=369&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=464&fit=crop&dpr=1 754w, https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=464&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/539192/original/file-20230725-15-mqxwrk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=464&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Compression socks can be helpful to treat lymphoedema.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/woman-putting-on-compression-stockings-legs-1884644173">Shutterstock</a></span>
</figcaption>
</figure>
<p>Lymphatic massage requires specialised training and an understanding of the lymphatic vessels. It involves stretching and stroking the skin to move fluid from the swollen region to a location where the lymphatic system is functioning properly.</p>
<p>Lymphatic massage can reduce lymphoedema associated with <a href="https://pubmed.ncbi.nlm.nih.gov/11519024/">cancer treatment</a>. An Australian study also reported that lymphatic massage reduced pain, depression and fatigue in <a href="https://pubmed.ncbi.nlm.nih.gov/35280240/">cancer patients</a>. </p>
<p>Increasing lymph flow back towards the heart is also essential to prevent complications like <a href="https://theconversation.com/whats-cellulitis-a-dermatologist-explains-185568">cellulitis</a> or skin infection. A proper diagnosis should precede any treatment for lymphoedema. </p>
<p>You might have seen social media posts or services promising to boost lymphatic drainage for <a href="https://www.healthline.com/health/lymphatic-drainage-face#beauty-benefits">relaxation, beauty or health reasons</a>. Lymphatic facial massage and traditional Chinese techniques of <a href="https://pubmed.ncbi.nlm.nih.gov/17905355/">gua sha</a> and jade rollers can increase blood flow and lymph flow, but need to be <a href="https://pubmed.ncbi.nlm.nih.gov/29998311/">used correctly</a>. </p>
<p>These treatments are best performed by someone who is trained in the anatomy of the lymphatic system and lymph flow. If you do try these yourself, light pressure is needed because the lymphatic vessels are only just under the skin. It is uncommon to have lymphoedema in the face, but increased blood flow to the skin and a nice massage are still beneficial. </p>
<p>To keep your lymphatic system <a href="https://www.healthdirect.gov.au/lymphoedema">working well</a>, it is important to exercise, maintain a healthy weight and eat a diet that is rich in antioxidants and not high in salt.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-does-my-back-get-so-sore-when-im-sick-the-connection-between-immunity-and-pain-207222">Why does my back get so sore when I'm sick? The connection between immunity and pain</a>
</strong>
</em>
</p>
<hr>
<h2>New promise for patients</h2>
<p>New research is examining artificial stimulation of new <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10178056/">lymphatic vessel</a> growth. </p>
<p>Better imaging techniques have allowed for clearer visualisation of the lymphatic pathways and increased understanding of the <a href="https://www.sciencedirect.com/science/article/pii/S0169409X20301241">lymphatic system</a>. </p>
<p>The lymphatic system may not be as mysterious as it once was. However, there is still much more to be learnt about the lymphatic system and its roles in health and disease.</p><img src="https://counter.theconversation.com/content/209334/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Laurencia Villalba is a vascular surgeon in private and public practice.</span></em></p><p class="fine-print"><em><span>Alison Tomlin and Theresa Larkin 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>Named after Greek and Roman mythical creatures, the lymph that flows around the body helps it fight off infection and maintain a fine balance of fluids.Theresa Larkin, Associate professor of Medical Sciences, University of WollongongAlison Tomlin, Senior lecturer, Faculty of Science, Medicine and Health, Graduate School of Medicine, University of WollongongLaurencia Villalba, Honorary fellow, Faculty of Science, Medicine and Health, Graduate School of Medicine, University of WollongongLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2104422023-08-02T20:39:28Z2023-08-02T20:39:28ZImmunity for witnesses is a key tool of prosecutors, whether they’re charging Trump or other alleged criminals – here’s how it works and what the limits are<figure><img src="https://images.theconversation.com/files/540826/original/file-20230802-26048-u6ul4j.jpg?ixlib=rb-1.1.0&rect=0%2C33%2C5580%2C3617&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">A protester walks past the E. Barrett Prettyman U.S. District Court House in Washington, on August 1, 2023.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/protester-walks-past-the-e-barrett-prettyman-u-s-district-news-photo/1586150197?adppopup=true">Anna Moneymaker/Getty Images</a></span></figcaption></figure><p><em>At the heart of the alleged scheme for which Donald Trump was indicted on Aug. 1, 2023, was a fake electors plot designed to help him hold onto power after losing the 2020 presidential election.</em></p>
<p><em>In the U.S., people known as electors from each state and Washington, D.C., elect the president based on the popular vote.</em></p>
<p><em>According to the four-count indictment, Trump and two of six unnamed co-conspirators pulled together fraudulent slates of electors in seven key states in an attempt to subvert the real electors who were obligated, based on results of the popular vote, to cast ballots for Joe Biden. The fake electors cast fraudulent ballots for Trump.</em> </p>
<p><em>This latest indictment represents the most serious charges against Trump yet.</em></p>
<p><em>In Fulton County, Georgia, where there is an investigation into alleged fake electors underway, a court filing indicates that District Attorney Fani Willis <a href="https://apnews.com/article/fulton-county-election-investigation-trump-georgia-fb5240cf854eb546b027f950646268c2">granted immunity to eight fake electors</a>. And it’s possible that special counsel Jack Smith acted similarly in the federal probe. Based on anonymous sources, <a href="https://www.cnn.com/2023/06/23/politics/special-counsel-fake-electors-immunity-testimony-jan-6/index.html">CNN reported that Smith compelled at least two fake electors</a> to testify before a Washington, D.C., grand jury by giving them limited immunity.</em></p>
<p><em>The Conversation U.S. asked legal scholar <a href="https://law.wayne.edu/profile/gb7147">William Ortman</a>, an associate professor of law at Wayne State University, to explain how immunity and limited immunity work.</em></p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Jack Smith wears a dark blue suit and a tie and is partially obscured by a dark wall." src="https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=415&fit=crop&dpr=1 600w, https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=415&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=415&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=522&fit=crop&dpr=1 754w, https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=522&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/540818/original/file-20230802-22768-6zixs7.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=522&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">Special counsel Jack Smith arrives to give remarks following the Aug. 1, 2023, indictment of former President Donald Trump.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/special-counsel-jack-smith-arrives-to-give-remarks-on-a-news-photo/1570193282?adppopup=true">Dave Angerer/Getty Images</a></span>
</figcaption>
</figure>
<h2>What does it mean when a witness is granted immunity?</h2>
<p>It depends on what kind of immunity we’re talking about. There are two basic types, which lawyers refer to as <a href="https://www.justice.gov/archives/jm/criminal-resource-manual-717-transactional-immunity-distinguished">transactional immunity and use immunity</a>. It’s easier to think of them as full immunity and limited immunity.</p>
<p>Full immunity is just what it sounds like. When a prosecutor grants a witness full immunity for an offense, she cannot thereafter prosecute the witness for that offense. Full immunity is tantamount to a “<a href="https://www.talksonlaw.com/briefs/what-is-immunity">get out of jail free</a>” card.</p>
<p>Limited immunity is more complicated. When a prosecutor grants a witness limited immunity, she <a href="https://supreme.justia.com/cases/federal/us/406/441/">can still prosecute</a> the witness. But she can’t use the witness’s immunized testimony, or evidence that comes from it, against the witness. </p>
<h2>Why would a prosecutor give a witness immunity?</h2>
<p>Prosecutors grant immunity when they want testimony from someone who has refused. Generally, the government <a href="https://supreme.justia.com/cases/federal/us/445/40/">can compel testimony</a> from anyone with information about a case.</p>
<p>The catch is that witnesses have a right under <a href="https://www.law.cornell.edu/wex/fifth_amendment">the Fifth Amendment</a> to refuse to answer questions that could be self-incriminating. That puts prosecutors in a bind, particularly when they want information that is in the hands – or the minds – of people who participated in the activity they are seeking to prosecute. </p>
<p>Immunity gives prosecutors a way out. If a person has immunity, then by definition their <a href="https://supreme.justia.com/cases/federal/us/406/441/">testimony cannot incriminate</a> them. That’s why if a witness has been granted immunity and refuses to testify, they can be <a href="https://www.justice.gov/archives/jm/criminal-resource-manual-728-criminal-contempt">held in contempt</a> and sent to jail.</p>
<h2>What does a witness get out of immunity?</h2>
<p>It again depends on what kind of immunity we’re talking about. For a witness concerned about being charged with a crime, the benefits of full immunity are obvious. Limited immunity is less attractive to defendants, but it is often still appealing. That’s because it can be difficult for <a href="https://casetext.com/case/united-states-v-hampton-2">prosecutors to establish</a> that they obtained evidence independent of immunized testimony, so limited immunity still offers witnesses some protection against future prosecution.</p>
<p>There are, however, hazards to testifying under a grant of immunity. One is that immunity typically <a href="https://law.justia.com/cases/federal/district-courts/FSupp/495/607/2008000/">does not cover perjury</a>. So if an immunized person testifies and lies, or if the prosecutor just thinks they lied, they could be charged with a crime after all. </p>
<p>Beyond the risk of a perjury charge, testifying often means that a witness must provide information that could send a friend or ally to prison. It also means that the witness will be cross-examined by a defense lawyer, who will likely try to <a href="https://forensicresources.org/wp-content/uploads/2021/05/Cross-examining-the-snitch.pdf">convince the jury</a> that the witness is lying. There is also the possibility that the defendant or his associates, or both, might retaliate against the witness <a href="https://casetext.com/case/piemonte-v-united-states-2">outside of the courthouse</a>.</p>
<h2>Is immunity negotiated between prosecutors and witnesses? How is it determined whether a witness gets full or limited immunity?</h2>
<p>The government can negotiate immunity with a witness, but it doesn’t have to. When immunity is negotiated, it looks a lot like a plea agreement, except that the potential defendant doesn’t plead guilty to a crime. Immunity deals can get complicated, but the basic terms are pretty simple: The government agrees that it will not prosecute the person, which is full immunity, or that it will not use the person’s testimony against them, which is limited immunity, while the person agrees to cooperate in some way, often by testifying.</p>
<p>That said, the government can grant immunity to compel a witness’s testimony, even if the witness objects. That makes sense when you recall that the primary function of immunity is to overcome a witness’s right to remain silent. Whether a witness receives full or limited immunity in those situations is determined by statutes and state constitutions. In the <a href="https://www.law.cornell.edu/uscode/text/18/6002">federal system</a> and <a href="https://www.illinoislawreview.org/wp-content/ilr-content/articles/2003/3/Clair.pdf">some states</a>, the prosecutor merely has to grant limited immunity to compel testimony. In other states, though, prosecutors can compel a person’s testimony only by granting full immunity.</p>
<figure class="align-center ">
<img alt="A gavel sits on a bare table, in front of an empty courtroom." src="https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/540820/original/file-20230802-20-tdfx92.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">It’s possible that special counsel Jack Smith granted immunity to fake electors or co-conspirators in the federal probe of former President Donald Trump.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/courtroom-and-gavel-royalty-free-image/876701606?phrase=court+witness+US&adppopup=true">imaginima/Getty Images</a></span>
</figcaption>
</figure>
<h2>Is there a difference between state and federal immunity?</h2>
<p>Some states are more generous than others, or than the federal government, in granting full rather than limited immunity. Beyond that, there are various procedural differences between state and federal immunity that can sometimes be important. But on the major points, there aren’t many glaring differences between how witness immunity works in the federal and state systems.</p>
<h2>Can granting immunity in one jurisdiction make the job of a prosecutor in another jurisdiction harder?</h2>
<p>Absolutely, and that is why federal and state prosecutors often coordinate. When a witness testifies in a state proceeding pursuant to a formal immunity grant from a state prosecutor, their testimony can’t be used against them in federal court either. In other words, the person has <a href="https://supreme.justia.com/cases/federal/us/378/52/">limited immunity in federal proceedings</a>. And it works the <a href="https://www.law.cornell.edu/uscode/text/18/6002">same way in reverse</a>. When a person testifies with immunity in a federal proceeding, that testimony cannot be used against them in a state prosecution. </p>
<p>That makes good sense. If a person’s testimony could be used against them at a different jurisdictional level, they would still be able to invoke the Fifth Amendment and refuse to answer questions. It can, however, complicate matters when prosecutors at one level try to prosecute a person who received immunity at a different level. One thing that trips up prosecutors in these situations is the requirement that to prosecute someone who has been given immunity they must establish that their evidence is independent of any immunized testimony. That can get tricky.</p><img src="https://counter.theconversation.com/content/210442/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>William Ortman 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>Immunity deals may play a key role in the prosecution of former President Donald Trump.William Ortman, Associate Professor of Law, Wayne State 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/2077242023-06-22T02:11:07Z2023-06-22T02:11:07ZDo I need a booster vaccine if I recently had COVID? What if I’m not sure what I had?<figure><img src="https://images.theconversation.com/files/533059/original/file-20230621-14332-ci9rr5.jpg?ixlib=rb-1.1.0&rect=38%2C7%2C5121%2C3435&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/officers-nurse-use-needles-suck-covid19-2090251705">Shutterstock</a></span></figcaption></figure><p>In early 2021, recommendations about COVID vaccines were pretty straightforward – get two doses, as soon as you are eligible. A year later, we knew getting a third dose <a href="https://www.nature.com/articles/s41591-022-01727-0">was important</a> for protection against the new Omicron variant. </p>
<p>Today, though, the situation is far more complex – new updated vaccines are available, the majority of Australians have <a href="https://kirby.unsw.edu.au/sites/default/files/COVID19-Blood-Donor-Report-Round3-Aug-Sep-2022.pdf">likely been infected</a> at least once with an Omicron strain, and waves of infection continue to occur. </p>
<p>So how should you manage and time your booster shots?</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/over-half-of-eligible-aged-care-residents-are-yet-to-receive-their-covid-booster-and-winter-is-coming-205403">Over half of eligible aged care residents are yet to receive their COVID booster. And winter is coming</a>
</strong>
</em>
</p>
<hr>
<h2>Why do vaccines need boosters?</h2>
<p>Vaccines work by training our body’s immune system to react harder, faster, stronger and better when we get infected by a pathogenic virus or bacteria. </p>
<p>Unfortunately, this protective benefit is not permanent and immunity tends to “wane” over time. The extent to which vaccine protection wanes is a function of two main factors. </p>
<p>First, your <a href="https://www.youtube.com/watch?v=la6nXuAw-Oo">immune system</a> (in the form of antibodies, memory B cells and T cells) is not infinite, and the levels of vaccine-induced immune responses will gradually decline over time. Second, pathogens circulating in the community can mutate, which enables “escape” from being recognised by the immune system. The more the virus escapes, the less protection the vaccine can give you.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-does-my-back-get-so-sore-when-im-sick-the-connection-between-immunity-and-pain-207222">Why does my back get so sore when I'm sick? The connection between immunity and pain</a>
</strong>
</em>
</p>
<hr>
<h2>Some vaccines need frequent boosting, others last forever</h2>
<p>Not all pathogens have the same ability to create or tolerate mutations. For viruses that change little (such as measles), your childhood vaccines remain highly protective and you might never need a booster. </p>
<p>In contrast, some viruses can rapidly and dramatically change (looking at you, influenza), quickly rendering our vaccines outdated and making updates necessary.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/i-need-a-flu-shot-and-a-covid-booster-can-i-get-them-at-the-same-time-204027">I need a flu shot and a COVID booster. Can I get them at the same time?</a>
</strong>
</em>
</p>
<hr>
<h2>So, where does COVID fit in?</h2>
<p>SARS-CoV-2, the virus that causes COVID, has demonstrated an ability to rapidly change since emerging in 2019. Although the early pandemic in Australia featured vaccine supply constraints, we now lucky to have many different vaccine options. </p>
<p>Recommendations currently favour updated mRNA “bivalent” boosters from Pfizer or Moderna, each containing equal parts of the original virus strain and an Omicron strain. </p>
<p>But the virus continues to change (currently XBB strains are <a href="https://www.health.nsw.gov.au/Infectious/covid-19/Documents/weekly-covid-overview-20230610.pdf#page=9">dominant</a>, and further updates to the composition of the vaccine are to be expected in the future (<a href="https://www.fda.gov/vaccines-blood-biologics/updated-covid-19-vaccines-use-united-states-beginning-fall-2023">most likely to target XBB.1.5</a>).</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1668393515670175744"}"></div></p>
<h2>That’s great, but I recently had COVID, so …</h2>
<p>Are you sure? Queuing for a PCR test seems like a fever dream from the past. Now, many of the RATs stacked in our cupboards are rapidly expiring. Influenza and RSV are <a href="https://www.abc.net.au/news/2023-05-08/rsv-flu-outbreak-hits-queensland-hard-cases-5-times-higher/102272112">back with gusto</a> (and cause similar symptoms). </p>
<p>If you did have confirmed COVID, <a href="https://www.cell.com/immunity/fulltext/S1074-7613(22)00238-2">our research</a> shows the majority of people mount a <a href="https://www.cell.com/immunity/fulltext/S1074-7613(23)00091-2">strong immune response</a> following each infection. </p>
<p>This means that once you recover, your immunity has been “updated” to reflect the virus variant that caused your infection and you will have higher protective antibody levels in your blood.</p>
<h2>Well, I definitely had something. What does that mean for my COVID booster?</h2>
<p>There are a couple of things to consider here. </p>
<p>Firstly, there is no such thing as “too much” immunity. Beyond the regular <a href="https://www.health.gov.au/our-work/covid-19-vaccines/advice-for-providers/clinical-guidance/adverse-events">side-effects of a vaccine</a>, there are no known additional risks to being re-vaccinated soon after an infection. </p>
<p>On the other hand, getting vaccinated quickly after recovery will not do much to further boost your immunity. <a href="https://www.health.gov.au/our-work/covid-19-vaccines/getting-your-vaccination/booster-doses">Current recommendations</a> are to wait six months after infection or your last dose before seeking another booster. </p>
<p>This allows your immune system time to rest, so that it can be effectively re-activated by vaccination. If you’d prefer to minimise your risk of COVID, and you don’t know what caused a recent illness, “<a href="https://www.health.gov.au/top-up-covid-19-protection">topping up</a>” your immunity via a booster may be the way to go.</p>
<h2>How should we balance booster shots and infections in the community?</h2>
<p>The short answer is, we need more information and time to figure that out. </p>
<p>Our communities now have high immunity (from both vaccines and infections), so balancing the risks and rewards of COVID boosters is increasingly complex. </p>
<p>Ultimately, your personal health care provider is best placed to offer specific advice. Generally however, those who are vaccinated (with three or more doses), younger (64 and under), and otherwise healthy have the least to gain.</p>
<p>For those who are older (especially over 65s) or who have health complications, regular COVID boosters are likely to be an important tool for staying healthy, especially over the winter season. While we still need more data, <a href="https://jamanetwork.com/journals/jama/fullarticle/2794072">multiple studies</a> suggest booster vaccines can <a href="https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00354-6/fulltext">reduce the risk</a> of developing long COVID, providing another reason to keep up-to-date. </p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1642752884738768898"}"></div></p>
<h2>The bottom line</h2>
<p>Unfortunately, COVID is among us and likely here for good. But like old mate influenza, we now have effective tools to blunt the impacts of COVID, and even better options will come through the pipeline to unlock further health improvements (like the transformative <a href="https://www.nature.com/articles/d41586-023-01529-5">new vaccines for RSV</a>). </p>
<p>For now, stay tuned to the latest <a href="https://www.health.gov.au/news/atagi-2023-booster-advice">advice from the Australian Technical Advisory Group on Immunisation</a> (ATAGI) about additional vaccine boosters and rest assured scientists and public health officials are still working to better understand how best to maintain high levels of population immunity via regular immunisation.</p><img src="https://counter.theconversation.com/content/207724/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Adam Wheatley receives funding from NHMRC, MRFF and ARC. </span></em></p><p class="fine-print"><em><span>Jennifer Juno receives funding from the NHMRC, MRFF and NIH.</span></em></p>Firstly, there is no such thing as ‘too much’ immunity. Beyond the regular side-effects of a vaccine, there are no known additional risks to being re-vaccinated soon after an infection.Adam Wheatley, Laboratory Head, Department of Microbiology and Immunology, The University of MelbourneJennifer Juno, Laboratory Head, The Peter Doherty Institute for Infection and ImmunityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2055172023-05-12T12:45:47Z2023-05-12T12:45:47ZObesity speeds up loss of immunity from COVID vaccines – new research<figure><img src="https://images.theconversation.com/files/525735/original/file-20230511-19-1r3lyn.jpg?ixlib=rb-1.1.0&rect=9%2C0%2C6221%2C4147&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/doctor-nurse-scientist-researcher-holding-flu-1805484811">iiiNooMiii/Shutterstock</a></span></figcaption></figure><p>COVID vaccines are very effective, but for some groups they don’t generate as strong an immune response. These groups include <a href="https://www.nature.com/articles/s41586-021-03739-1">older adults</a> and people with weakened immune systems, for example due to <a href="https://www.nature.com/articles/s41571-022-00610-8">cancer</a> or other medical conditions. They tend to already be at heightened risk from COVID.</p>
<p>Likewise, <a href="https://www.thelancet.com/journals/landia/article/PIIS2213-8587(21)00089-9/fulltext">obesity</a> – and its association with several other conditions such as type 2 diabetes, high blood pressure and chronic kidney disease – leads to an increased risk of severe COVID.</p>
<p>The effect of obesity on COVID vaccine effectiveness, however, has not been well understood. But our new study in <a href="https://doi.org/10.1038/s41591-023-02343-2">Nature Medicine</a> finds obesity is linked to faster loss of immunity from COVID vaccines. </p>
<p>We know <a href="https://www.sciencedirect.com/science/article/abs/pii/S0264410X15009184">people with obesity</a> have an <a href="https://www.nature.com/articles/ijo2011208">impaired immune response</a> to other vaccines including those for influenza, rabies and hepatitis.</p>
<p>COVID vaccines generate antibodies which recognise the spike protein, a protein on the surface of SARS-CoV-2 (the virus that causes COVID) that allows it to attach to and infect our cells. The vaccines also prime immune cells called <a href="https://www.nature.com/articles/s41590-021-01122-w">T cells</a> to protect against severe COVID if we do contract the virus.</p>
<p>Because immunity acquired after two doses wanes <a href="https://www.nejm.org/doi/full/10.1056/nejmoa2114228">in the months afterwards</a>, many countries have elected to administer booster vaccines to maintain immune protection, particularly in vulnerable groups.</p>
<p>Several studies <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2022.839922/full">have suggested</a> that following <a href="https://onlinelibrary.wiley.com/doi/10.1002/oby.23417">COVID vaccination</a>, antibody levels <a href="https://www.mdpi.com/2227-9059/10/2/204">may be lower</a> in people with obesity than in the general population.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/severe-covid-in-young-people-can-mostly-be-explained-by-obesity-new-study-159072">Severe COVID in young people can mostly be explained by obesity – new study</a>
</strong>
</em>
</p>
<hr>
<p>Earlier in the pandemic, we assembled a team of researchers from the University of Cambridge and the University of Edinburgh to investigate the effect of obesity on vaccine effectiveness over time. </p>
<p>Using <a href="https://www.ed.ac.uk/usher/eave-ii">a data platform</a> called EAVE II, the University of Edinburgh team, led by Aziz Sheikh, examined real-time healthcare data for 5.4 million people across Scotland. In particular, they looked at hospitalisations and deaths from COVID among 3.5 million adults who had received two vaccine doses (either Pfizer or AstraZeneca).</p>
<p>They found that people with severe obesity, defined as a body mass index (BMI) over 40, had a 76% increased risk of hospitalisation and death from COVID after vaccination compared to those with a BMI in the normal range. The risk was also moderately increased in people who were obese (a BMI between 30 and 40) and those who were underweight (a BMI lower than 18.5).</p>
<p>The risk of severe disease from breakthrough infections after the second vaccine also began to increase more quickly among people with severe obesity (from around ten weeks post-vaccination) and among people with obesity (from around 15 weeks) compared with people of a normal weight (from around 20 weeks).</p>
<figure class="align-center ">
<img alt="A woman standing on scales." src="https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/525736/original/file-20230511-29-hulhqs.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">Obesity is a risk factor for severe COVID.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/woman-standing-on-scales-weight-loss-1520942567">Pixel-Shot/Shutterstock</a></span>
</figcaption>
</figure>
<h2>Investigating further</h2>
<p>Our team conducted experiments to characterise the immune response to a third dose, or booster, of mRNA COVID vaccines (those made by Pfizer and Moderna) in people with severe obesity.</p>
<p>We studied 28 people with severe obesity attending Addenbrooke’s Hospital in Cambridge, and measured antibody levels and function as well as the number of immune cells in their blood post-vaccination. We compared the results to those from 41 people of a normal weight.</p>
<p>Although antibody levels were similar in samples from all participants before booster vaccination, the ability of antibodies to work efficiently to fight the virus, known as “neutralisation capacity”, was reduced among people with severe obesity. In 55% of people with severe obesity we either couldn’t detect or quantify neutralisation capacity, compared to 12% of people with normal BMI.</p>
<p>This might mean COVID vaccines induce lower quality antibodies in people with obesity. It’s possible the antibodies are not able to bind to the virus with the same strength as in people of a normal weight.</p>
<hr>
<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/how-much-immunity-do-we-get-from-a-covid-infection-large-study-offers-new-clues-200044">How much immunity do we get from a COVID infection? Large study offers new clues</a>
</strong>
</em>
</p>
<hr>
<p>After a booster, antibody function in people with obesity was restored to the same level as those of normal weight. However, using detailed measurements of B cells, which are responsible for antibody production and immune memory, we found that these immune cells developed differently in the first couple of weeks after vaccination in people with obesity. </p>
<p>By repeating measurements of immune responses over time, we could see antibody levels and function declined more rapidly after the third dose in people with severe obesity. </p>
<h2>What does this mean?</h2>
<p>There were some limitations in both parts of the study. For example, BMI data was only collected once in EAVE II and therefore we cannot exclude changes in BMI over time. Also, the number of people included in our in-depth immunology study was relatively modest. </p>
<p>Nonetheless, immunity from COVID vaccines doesn’t seem to be as robust or long-lasting in people with obesity. With <a href="https://www.worldobesity.org/">severe obesity</a> affecting 3% of the UK population and 9% of the US population, these findings have important implications. </p>
<p>First, COVID boosters may be particularly important for this group. Our study also highlights the need for more targeted interventions to protect people with obesity from severe COVID. </p>
<p>Evidence shows weight loss of at least 5% can reduce the risk of type 2 diabetes and other <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5497590/">metabolic complications</a> of obesity. Interventions that can lead to a sustained reduction in weight (such as lifestyle modification, weight loss drugs, and bariatric surgery) could similarly improve COVID outcomes. </p>
<p>Weight loss may likewise improve vaccine responses, but we need more research to investigate.</p><img src="https://counter.theconversation.com/content/205517/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Agatha A. van der Klaauw received funding from ZonMW (2007, The Netherlands), Wellcome Trust (2012, UK) and UKRI (2021, UK). </span></em></p><p class="fine-print"><em><span>I. Sadaf Farooqi is supported by Wellcome (207462/Z/17/Z), Botnar Fondation, the Bernard Wolfe Health Neuroscience Endowment and a NIHR Senior Investigator Award. I. Sadaf Farooqi has consulted for Eli Lilly, Novo Nordisk and Rhythm Pharmaceuticals on weight loss drugs.
</span></em></p><p class="fine-print"><em><span>James E. D. Thaventhiran does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>We found the protection offered by COVID vaccines wanes more quickly in people with severe obesity compared to those of normal weight.Agatha A. van der Klaauw, Clinical Lecturer in Metabolic Medicine, University of CambridgeI. Sadaf Farooqi, Wellcome Principal Research Fellow and Professor of Metabolism and Medicine, University of CambridgeJames E. D. Thaventhiran, Researcher, MRC Toxicology Unit, University of CambridgeLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2025532023-03-30T15:20:57Z2023-03-30T15:20:57ZHay fever: why some people suffer from it and others don’t<figure><img src="https://images.theconversation.com/files/518169/original/file-20230329-28-d70vsm.jpg?ixlib=rb-1.1.0&rect=0%2C11%2C7360%2C4891&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/vibrant-blonde-middle-aged-woman-sneeze-622469891">Octa corp/Shutterstock</a></span></figcaption></figure><p>While the arrival of spring brings blooming flowers and trees, it also marks the beginning of allergy season for many people. Those who suffer from hay fever may start to notice <a href="https://www.nhs.uk/conditions/hay-fever/">familiar symptoms</a> such as sneezing, itchy eyes and a runny nose. </p>
<p>Hay fever, also known as allergic rhinitis, affects up to <a href="https://europepmc.org/article/med/17153005">42% of people</a> and can significantly impact their quality of life during the spring and summer months.</p>
<p>When a person with hay fever comes into contact with an allergen (pollen), their immune system mistakenly identifies it as a threat and produces an antibody called <a href="https://bestpractice.bmj.com/topics/en-gb/232">immunoglobulin E</a>, or IgE, to neutralise it. The IgE antibodies then attach themselves to a type of immune cells called mast cells, which are found in the nose, eyes and lungs. </p>
<p>When the allergen comes into contact with the IgE antibodies on the mast cells, it triggers the release of histamine and other proteins, causing inflammation and the symptoms of hay fever.</p>
<p>But why do so many people get hay fever, while others don’t? There are a range of factors at play.</p>
<h2>Genetics, immunity and the environment</h2>
<p>Genetic factors play a significant role in determining a person’s <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3151648/">susceptibility to hay fever</a>. Several genes, including those involved in immune system regulation and response, have been linked to an increased risk of developing hay fever. </p>
<p>Research has shown that the heritability – that is, the degree to which differences in people’s genes account for variations in their traits – ranges from <a href="https://www.frontiersin.org/articles/10.3389/fgene.2020.00270/full">33% to 91%</a> for hay fever. So, if people in your family have hay fever, you’re more likely to have it too.</p>
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Read more:
<a href="https://theconversation.com/do-i-have-covid-or-hay-fever-heres-how-to-tell-188030">Do I have COVID or hay fever? Here’s how to tell</a>
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<p>Some people’s immune systems <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573758/">may overreact to allergens</a>, leading to an allergic response and the development of hay fever. In fact, having other allergies, asthma, allergic dermatitis or eczema can <a href="https://www.mayoclinic.org/diseases-conditions/hay-fever/symptoms-causes/syc-20373039">increase your risk</a> of developing hay fever.</p>
<p>Environmental factors such as exposure to <a href="https://acaai.org/allergies/allergic-conditions/hay-fever/">air pollution, tobacco smoke and other irritants</a> may also make a person more susceptible to hay fever. This can be due to damage to the nasal passages and respiratory system, making it easier for allergens to enter the body and trigger an allergic response. Similarly, <a href="https://bmcpediatr.biomedcentral.com/articles/10.1186/1471-2431-10-61">exposure to second-hand smoke</a> in early life is a risk factor for later development of hay fever.</p>
<p>Some people may be <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5346329/">exposed to allergens</a> more frequently or in larger amounts than others, making them more susceptible to developing hay fever. This can be due to living in an area with high levels of pollen or being exposed to certain allergens at work, for example.</p>
<h2>Why can symptoms be worse in some seasons more than others?</h2>
<p>The amount of pollen or other allergens in the air can vary from year to year and season to season. In some years, the pollen count may be higher, leading to more severe hay fever symptoms.</p>
<p>Weather conditions, such as temperature, humidity and wind, <a href="https://link.springer.com/article/10.1007/s00484-017-1457-3">can affect</a> the amount and distribution of pollen in the air. A rainy spring may wash away some of the pollen, while a warm, dry summer may lead to more pollen production.</p>
<p>The body’s immune system can also change over time, which can affect how it responds to allergens. This means someone who had severe hay fever symptoms in the past may experience milder symptoms as they get older.</p>
<p>Indeed, hay fever can develop at any age, but it’s more common in <a href="https://onlinelibrary.wiley.com/doi/abs/10.1111/all.12002?casa_token=PWxI6ub0HtcAAAAA:a4GPzguEcA3aYK9Fu52clDTxPGFXsDuWml80jtViPIg8ilQDIcgOj58wwxcShXoz6q2br7L6eDAQ">children and young adults</a>. As a person ages, their immune system may become less reactive to allergens, leading to <a href="https://www.karger.com/article/Abstract/237398">a reduction in hay fever symptoms</a>.</p>
<figure class="align-center ">
<img alt="A young boy rubs his eyes." src="https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/518172/original/file-20230329-14-vosz9f.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Hay fever is common in children.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/boy-rubbing-eye-child-pollen-allergy-2155315549">Dragana Gordic/Shutterstock</a></span>
</figcaption>
</figure>
<p>People may be exposed to different allergens in <a href="https://link.springer.com/article/10.1007/s00484-017-1457-3">different years or seasons</a>, which can affect the severity of their symptoms. For example, someone who is allergic to grass pollen will be triggered at different times to those triggered by certain tree pollen.</p>
<p>Lifestyle factors such as stress, diet and exercise <a href="https://www.sciencedirect.com/science/article/pii/S0006899314014735?casa_token=H5zT4lQU1WwAAAAA:BiRy8aE-6zJT08dG5V5SDgo451zVC1wUFsAw67n0VwWXB58anEQ9n_rR5iiXyTLycoqT-2o">can affect the immune system</a> and may contribute to the severity of hay fever symptoms. For example, stress can weaken the immune system, making it <a href="https://www.immunology.theclinics.com/article/S0889-8561(10)00080-9/fulltext">more susceptible to allergens</a>. </p>
<p>Climate change is also altering the quantity and composition <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/all.14476">of pollen</a> that plants release, as well as the timing. Increasing temperatures and atmospheric carbon dioxide levels are causing some plants <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/j.1365-2222.2004.02061.x">to produce more pollen</a>, while other species are shifting their flowering periods to earlier in the year. This means pollen seasons are starting earlier, lasting longer, and becoming more intense.</p>
<h2>Tips for managing hay fever</h2>
<p><strong>Avoid allergens:</strong> Try to <a href="https://www.uptodate.com/contents/trigger-avoidance-in-allergic-rhinitis-beyond-the-basics">avoid exposure to allergens</a> that trigger your hay fever symptoms. This may mean staying indoors during high pollen counts or wearing a mask if you’re working outdoors.</p>
<p><strong>Use air filters:</strong> Consider using <a href="https://www.sciencedirect.com/science/article/pii/S0091674909013177?casa_token=CkTL0kWie5kAAAAA:yvBLfFgn9XJPlenxxkLdy4zPxxbXRorx0dDamOIaE6oYYlg4o_o0xn4Ay9IzbhcsJSpF1dE">Hepa (high-efficiency particulate air) air filters</a> in your home or workplace to help remove allergens from the air. </p>
<p><strong>Keep windows closed:</strong> <a href="https://www.nhs.uk/conditions/hay-fever/">Closing windows</a> during high pollen counts will prevent allergens from entering your home.</p>
<p><strong>Take antihistamines:</strong> These are <a href="https://www.nhs.uk/medicines/cetirizine/">medications</a> that help reduce hay fever symptoms by blocking the effects of histamine, which is released during an allergic reaction.</p>
<p><strong>Consider immunotherapy:</strong> <a href="https://www.ncbi.nlm.nih.gov/books/NBK279487/">Immunotherapy</a>, also known as allergy shots, can help reduce hay fever symptoms by desensitising your immune system to specific allergens over time.</p>
<p><strong>Manage stress:</strong> Stress <a href="https://journals.sagepub.com/doi/pdf/10.1177/1559827610395467?casa_token=FsgTLcz27JEAAAAA:7DCZvxNdzd184MqZ2VLQ5rmaZQ6vU00NUJ6UR8fLDeX6YrEBf43gst7eUMp30OrA5qc6hjAJfQ">can make hay fever symptoms worse</a>, so try to manage it through techniques such as meditation, yoga or deep-breathing exercises.</p>
<p>It’s important to talk to your doctor before starting any new medications or treatments for hay fever.</p><img src="https://counter.theconversation.com/content/202553/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>Our genetics, immune systems and conditions in the environment around us can all play a role in susceptibility to hay fever.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/2019022023-03-24T15:49:30Z2023-03-24T15:49:30ZCould the common cold give children immunity against COVID? Our research offers clues<figure><img src="https://images.theconversation.com/files/516450/original/file-20230320-2149-tvxyat.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C5399%2C3892&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/kids-playing-cheerful-park-outdoors-concept-419185651">Rawpixel.com/Shuttersock</a></span></figcaption></figure><p>Why children are less likely to become severely ill with COVID compared with adults is not clear. Some have suggested that it might be because children are less likely to <a href="https://www.sciencedirect.com/science/article/pii/S2666379122000659">have diseases</a>, such as type 2 diabetes and high blood pressure, that are known to be linked to more severe COVID. Others have suggested that it could be because of a difference in <a href="https://www.sciencedirect.com/science/article/pii/S1521661620307488?via%3Dihub">ACE2 receptors</a> in children – ACE2 receptors being the route through which the virus enters our cells.</p>
<p>Some scientists have also suggested that children may have a higher level of existing immunity to COVID compared with adults. In particular, this immunity is thought to come from <a href="https://www.nature.com/articles/s41577-022-00809-x">memory T cells</a> (immune cells that help your body remember invading germs and destroy them) generated by common colds – some of which are caused by coronaviruses.</p>
<p>We put this theory to the test in a <a href="https://www.pnas.org/doi/10.1073/pnas.2220320120">recent study</a>. We found that T cells previously activated by a coronavirus that causes the common cold recognise SARS-CoV-2 (the virus that causes COVID) in children. And these responses declined with age.</p>
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Read more:
<a href="https://theconversation.com/does-covid-really-damage-your-immune-system-and-make-you-more-vulnerable-to-infections-the-evidence-is-lacking-197253">Does COVID really damage your immune system and make you more vulnerable to infections? The evidence is lacking</a>
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<p>Early in the pandemic, scientists observed the presence of memory T cells able to recognise SARS-CoV-2 in people who had never been exposed to the virus. Such cells are often called cross-reactive T cells, as they stem from past infections due to pathogens other than SARS-CoV-2. Research has suggested these cells may provide some <a href="https://www.nature.com/articles/s41577-022-00809-x">protection against COVID</a>, and even enhance responses to COVID vaccines.</p>
<h2>What we did</h2>
<p>We used blood samples from children, sampled at age two and then again at age six, before the pandemic. We also included adults, none of whom had previously been infected with SARS-CoV-2.</p>
<p>In these blood samples, we looked for T cells specific to one of the coronaviruses that causes the common cold (called OC43) and for T cells that reacted against SARS-CoV-2.</p>
<p>We used an advanced technique called <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2019.01515/full">high-dimensional flow cytometry</a>, which enabled us to identify T cells and characterise their state in significant detail. In particular, we looked at T cells’ reactivity against OC43 and SARS-CoV-2.</p>
<p>We found SARS-CoV-2 cross-reactive T cells were closely linked to the frequency of OC43-specific memory T cells, which was higher in children than in adults. The cross-reactive T cell response was evident in two-year-olds, strongest at age six, and then subsequently became weaker with advancing age. </p>
<p>We don’t know for sure if the presence of these T cells translates to <a href="https://www.nature.com/articles/s41577-022-00809-x">protection against COVID</a>, or how much. But this existing immunity, which appears to be especially potent in early life, could go some way to explaining why children tend to fare better than adults with a COVID infection.</p>
<figure class="align-center ">
<img alt="A little boy sleeps with a teddy bear." src="https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/516453/original/file-20230320-1833-16if7k.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Children are less likely to get very sick from COVID than adults.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/photo-baby-boy-sleeping-together-teddy-1507922393">Dragana Gordic/Shutterstock</a></span>
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<h2>Some limitations</h2>
<p>Our study is based on samples from adults (26-83 years old) and children at age two and six. We didn’t analyse samples from children of other ages, which will be important to further understand age differences, especially considering that the mortality rate from COVID in children is lowest from ages five to nine, and <a href="https://www.nature.com/articles/s41586-020-2918-0">higher in younger children</a>. We also didn’t have samples from teenagers or adults younger than 26. </p>
<p>In addition, our study investigated T cells circulating in the blood. But immune cells are also found in other parts of the body. It remains to be determined whether the age differences we observed in our study would be similar in samples from the <a href="https://www.nature.com/articles/s41590-022-01292-1">lower respiratory tract</a> or <a href="https://www.science.org/doi/10.1126/sciimmunol.abk0894">tonsil tissue</a>, for example, in which T cells reactive against SARS-CoV-2 have also been detected in adults who haven’t been exposed to the virus.</p>
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Read more:
<a href="https://theconversation.com/colds-flu-and-covid-how-diet-and-lifestyle-can-boost-your-immune-system-197151">Colds, flu and COVID: how diet and lifestyle can boost your immune system</a>
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<p>Nonetheless, this study provides new insights into T cells in the context of COVID in children and adults. Advancing our understanding of memory T cell development and maturation could help guide future vaccines and therapies.</p><img src="https://counter.theconversation.com/content/201902/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Marion Humbert received funding from KI Foundation for Virus Research (Karolinsk Institutet, Sweden) and Läkare mot AIDS (Sweden).</span></em></p><p class="fine-print"><em><span>Annika Karlsson receives funding from the Swedish Research Council (Dnr 2020-02033), CIMED project grant, senior (Dnr: 20190495), and Karolinska Institutet (Dnr: 2019-00931 and 2020-01599). </span></em></p>Certain immune cells acquired from a coronavirus that causes the common cold appear to react to COVID – but more so in children that adults.Marion Humbert, Postdoctoral Researcher in Immunology, Karolinska InstitutetAnnika Karlsson, Researcher, Department of Laboratory Medicine, Karolinska InstitutetLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2021512023-03-23T07:51:28Z2023-03-23T07:51:28ZTB kills 75,000 children in Africa every year: how this can stop<figure><img src="https://images.theconversation.com/files/516948/original/file-20230322-26-dpm8er.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">There have been substantial improvements in some areas of TB therapeutics. </span> <span class="attribution"><span class="source">Punit Paranjpe/AFP via Getty Images</span></span></figcaption></figure><p><em>Tuberculosis (TB) is a preventable and curable disease. Half of the world’s 30 highest TB burden countries are in Africa. In many of these countries, TB is the leading cause of death across age groups, but especially among children. Globally, TB is the <a href="https://www.who.int/teams/global-tuberculosis-programme/tb-reports/global-tuberculosis-report-2022/tb-disease-burden/2-2-tb-mortality">leading cause of death</a> by any single infectious agent (above COVID-19 and HIV).</em></p>
<p><em>The people most affected by TB are often the most socio-economically marginalised, with the fewest reserves to take them through the treatment journey. This is extremely challenging, with complex, often delayed diagnosis, many months of treatment, and often long-term effects after treatment. The Conversation Africa’s Ina Skosana spoke to Graeme Hoddinott, a socio-behavioural science lead at the Desmond Tutu TB Centre, Stellenbosch University, and an African Academy of Sciences ARISE Fellow.</em></p>
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<h2>What’s the TB burden among young people?</h2>
<p>In Africa, of the <a href="https://www.who.int/teams/global-tuberculosis-programme/tb-reports/global-tuberculosis-report-2022/tb-disease-burden/2-1-tb-incidence">three million people</a> who develop TB disease every year, nearly 160,000 are children 0-4 years old, and another 160,000 are 5-14 years old. Every year, about <a href="https://www.who.int/teams/global-tuberculosis-programme/tb-reports/global-tuberculosis-report-2022/tb-disease-burden/2-2-tb-mortality">500,000 people in Africa</a> die because of TB. Children make up 15% (75,000) of these deaths. </p>
<p>Less than half of the children aged 0-14 who have TB are diagnosed – so they never even start treatment.</p>
<h2>What are some of the drivers?</h2>
<p>TB is transmitted between people through the air. When a person with TB coughs or breathes out, some of the TB bugs are expelled to float in the air. If someone else then breathes the bugs in, they cause a new infection. There are several factors that increase the risk of TB transmission. These include actions that increase the number of bugs in the air, such as not wearing a mask and coughing more. And actions that increase exposure, such as spending long periods of time breathing the air in. </p>
<p>A person might breathe the TB bugs in (that is, become infected), but not become ill. This is known as latent TB. Sometimes, though, the TB bugs are able to multiply and escape the body’s immune system. As the number of bugs increases, the person begins to experience symptoms such as coughing, drenching sweats and weight loss. This is then called TB disease. </p>
<p>A variety of factors increase the risk of progressing from TB infection to disease. These are factors that might impede the body’s natural immune functioning, such as undernourishment or smoking. </p>
<p>Children (especially young children) have less developed immune systems. This makes their chance of progressing from infection to disease higher than it is for adults. </p>
<p>Prevention of infection can be done through reducing risks of transmission, for example by opening windows to allow the bugs to blow away. Also, if a person with TB is on treatment, then the number of bugs they expel is dramatically reduced. That’s why it’s important to get an early diagnosis and start treatment.</p>
<p>Where there is an exposure risk, we can also use medicines to reduce the chance of developing disease – this is called TB preventive therapy. The most recent World Health Organization <a href="https://apps.who.int/iris/bitstream/handle/10665/331170/9789240001503-eng.pdf">guidelines</a> suggest that preventive therapy be offered to everyone who has significant exposure risk to an adult or adolescent with TB. For example, think about young children who are sharing a bed with their mother. If she has TB, then the child should be offered preventive therapy, as should other people who share their home. </p>
<p>Unfortunately, in most settings in Africa, implementation of TB preventive therapy is either non-existent or extremely sub-optimal. Historically, the only available TB preventive regimen was a once-daily treatment for six months that is burdensome to administer; new regimens are becoming available. Unfortunately, the limited resources available to TB services have prioritised TB treatment and not prevention. </p>
<h2>Where are the gaps?</h2>
<p>There have been <a href="https://www.nejm.org/doi/10.1056/NEJMoa2104535">substantial</a> <a href="https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-017-2377-x">improvements</a> in some areas of <a href="https://www.ingentaconnect.com/content/iuatld/ijtld/2023/00000027/00000003/art00005;jsessionid=2sjtfaionun19.x-ic-live-03">TB therapeutics</a>, with <a href="https://erj.ersjournals.com/content/48/5/1503">shorter</a>, more <a href="https://www.ingentaconnect.com/content/iuatld/ijtld/2023/00000027/00000002/art00006">palatable</a> regimens and more <a href="https://www.ingentaconnect.com/content/iuatld/ijtld/2023/00000027/00000001/art00005">easy-to-use</a> <a href="https://www.ingentaconnect.com/content/iuatld/ijtld/2022/00000026/00000012/art00006">formulations</a>. However, these are not universally available and are still not optimal. Even “shorter” treatment is four months long. Health systems are poorly equipped to support continuity of care when patients (including children and adolescents) move between facilities.</p>
<p>Far too many children who initiate both TB preventive therapy and TB treatment <a href="https://www.jahonline.org/article/S1054-139X(22)00778-9/fulltext">are lost</a> to <a href="https://www.ingentaconnect.com/content/iuatld/pha/2022/00000012/00000004/art00003">follow-up</a>. TB programmes across the world have yet to operationalise the high-minded ideals of “<a href="https://journals.plos.org/globalpublichealth/article?id=10.1371/journal.pgph.0001357">patient-centred care</a>”. The experiences of adolescents and young people (10-24 years old) accessing TB services are often especially <a href="https://www.jahonline.org/article/S1054-139X(22)00778-9/fulltext">problematic</a>. For example, <a href="https://www.mdpi.com/2076-0817/10/12/1591">adolescents report</a> being assumed to have HIV, being shouted at for being sexually active (even if they are not) and being told to access TB services at times when they are in <a href="https://journals.plos.org/globalpublichealth/article?id=10.1371/journal.pgph.0000989">school</a>. </p>
<p>There is also limited integration between health services and other sectors (like basic education) to make care easier to get. There remain <a href="https://www.ingentaconnect.com/content/iuatld/ijtld/2017/00000021/a00111s1/art00013">high rates</a> of TB-associated <a href="https://bmcmedicine.biomedcentral.com/articles/10.1186/s12916-019-1250-8">stigma</a>, and the <a href="https://bmcpulmmed.biomedcentral.com/articles/10.1186/s12890-018-0777-3">costs of TB care</a> (economic, social and psychological) can be <a href="https://thorax.bmj.com/content/76/4/387">catastrophic and long-lasting</a>. </p>
<h2>How must TB programmes be tailored?</h2>
<p>A fraction of the funding and collective effort that was mobilised for COVID-19 could realistically push towards TB elimination. Perversely, instead, resources redirected towards COVID-19 have <a href="https://www.theglobalfund.org/en/news/2021/2021-09-08-global-fund-results-report-reveals-covid-19-devastating-impact-on-hiv-tb-and-malaria-programs/">set the global TB programme back</a> by a decade’s worth of progress. </p>
<p>TB programmes must be tailored by listening to the preferences and priorities of people affected by TB, by working to address the real-world limitations experienced by frontline health services, and by continuing to develop better, more acceptable therapeutics; especially medicines that are more acceptable for children and easier for caregivers to prepare and administer. </p>
<p>But really all of that can only make a big difference if we all wake up to this leading cause of death, especially among children, and care more.</p><img src="https://counter.theconversation.com/content/202151/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Graeme Hoddinott is a fellow of the African Research Initiative for Scientific Excellence (ARISE) programme. His ARISE research is focused on optimising care for adolescents with tuberculosis. The ARISE programme is implemented by the African Academy of Sciences (AAS) with support from the European Commission and the African Union Commission.</span></em></p>Less than half of the children aged 0-14 who have TB are diagnosed – so they never even start treatment.Graeme Hoddinott, Socio-behavioural Scientist and Senior Researcher, Stellenbosch UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/2000442023-02-17T14:27:30Z2023-02-17T14:27:30ZHow much immunity do we get from a COVID infection? Large study offers new clues<figure><img src="https://images.theconversation.com/files/510863/original/file-20230217-452-9keo34.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C3761%2C2503&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/variety-passengers-ride-subway-car-1879740988">SmartPhotoLab/Shutterstock</a></span></figcaption></figure><p>After a COVID infection, whether it’s a first, second, or even a third, many of us wonder how long we might be protected against a reinfection, and whether we’ll be susceptible to new variants. Also, if we do catch COVID again, will the immunity we’ve acquired from this infection reduce the severity of the next one?</p>
<p>A <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)02465-5/fulltext">new study</a> published in The Lancet set out to answer these questions, looking at the strength and duration of natural immunity by COVID variant.</p>
<p>The authors collected data from 65 studies across 19 countries, making it the largest review on this topic to date. These studies compared COVID risk among people who had been infected previously and those without a prior infection. Studies looking at natural immunity in combination with vaccination (hybrid immunity) were excluded.</p>
<p>The researchers aimed to assess if infection induced similar protection against reinfection with different variants, and if this waned differently over time.</p>
<p>The analyses spanned studies from the beginning of the pandemic until September 2022, and looked primarily at the alpha, beta, delta and omicron BA.1 variants. </p>
<h2>Protection from reinfection</h2>
<p>The authors evaluated protection against reinfection, symptomatic disease, and severe disease (defined as hospitalisation or death) separately. </p>
<p>They found previous infection was highly protective against reinfection with alpha, beta and delta variants, but less so against omicron BA.1. A previous infection provided moderate protection from reinfection with omicron BA.1 (45%), compared with stronger protection against pre-omicron variants (82%). This was also the case for symptomatic infection. </p>
<p>Data from long-term studies showed that protection against reinfection for pre-omicron variants dropped to 78.6% over 40 weeks, whereas for omicron BA.1 it dropped more rapidly to 36.1%.</p>
<p>When assessing severe disease, however, all variants showed sustained protection above 88% for 40 weeks. This isn’t to say that protection drops substantially after 40 weeks. Rather, it seems there was limited data available that followed people for long enough for the authors to be able to draw strong conclusions beyond this time frame.</p>
<p>The results also revealed that protection against severe disease after natural infection was comparable to that received from two vaccine doses, for both pre-omicron and omicron BA.1 variants.</p>
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Read more:
<a href="https://theconversation.com/genetics-might-explain-why-some-people-have-never-had-covid-but-we-shouldnt-be-too-focused-on-finding-out-198108">Genetics might explain why some people have never had COVID – but we shouldn't be too focused on finding out</a>
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<h2>Making sense of the findings</h2>
<p>A couple of years is a long time for highly contagious respiratory viruses, and SARS-CoV-2 (the virus that causes COVID) has been no different. It has generated sequential variants of concern, with increased transmissibility and capacity to evade our immune responses compared with the ancestral virus. </p>
<p>The study’s observations, which treat protection against pre-omicron variants and omicron BA.1 separately, make sense when we consider how <a href="https://www.nature.com/articles/s41586-022-04474-x">omicron variants differ</a> from their predecessors. </p>
<p>By way of background, neutralising antibodies generated after previous viral infection are important to prevent subsequent virus entry to susceptible cells. These Y-shaped molecules recognise intact proteins of the virus exterior and attach to them, preventing the virus from latching on to the cell receptor necessary for infection. </p>
<p>But to persist, viruses like SARS-CoV-2 introduce random mutations in their genome when they replicate, aiming to continuously alter their proteins to escape immune recognition.</p>
<p>Omicron lineages have enough mutations to differentiate substantially from previous variants, and therefore <a href="https://www.cell.com/cell/fulltext/S0092-8674(21)01578-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867421015786%3Fshowall%3Dtrue">evade existing antibodies</a>. Evasion from neutralising antibodies explains our failure to control reinfection by omicron variants. </p>
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<img alt="An illustration of SARS-CoV-2, the virus that causes COVID." src="https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=337&fit=crop&dpr=1 600w, https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=337&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=337&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/510865/original/file-20230217-28-rth3o0.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">
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<span class="caption">SARS-CoV-2 has evolved significantly.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-illustration/sarscov2-coronavirus-virus-which-causes-covid19-1687909633">Kateryna Kon/Shutterstock</a></span>
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<p>Thankfully, we don’t just rely on antibodies for protection. A type of immune cells called <a href="https://www.nature.com/articles/s41590-021-01122-w">T cells</a> recognise snippets of virus proteins rather than intact proteins. This means it would take many more mutations in the virus genome to completely evade T cell immunity. </p>
<p>Unlike antibodies, T cells don’t seek out viruses. Instead they recognise infected cells and rapidly eliminate them to reduce virus factories in the body. T cells therefore act where neutralising antibodies may have failed, after infection. A robust T cell response to coronaviruses is crucial to prevent severe disease, and fortunately, tougher for omicron to evade. </p>
<p>SARS-CoV-2-specific T cells <a href="https://onlinelibrary.wiley.com/doi/10.1111/imr.13089">wane more slowly</a> than antibodies. In fact, people infected with the similar coronavirus SARS in 2003 <a href="https://www.nature.com/articles/s41586-020-2550-z">still had T cells</a> which recognise SARS-CoV-2 17 years after infection.</p>
<h2>Infection versus vaccination</h2>
<p>While a natural infection may offer equivalent protection to vaccination, this is not to say you should seek to become infected. SARS-CoV-2 remains a dangerous and unpredictable virus which can, in some cases, cause a host of damaging effects that linger long after recovery.</p>
<p>The authors suggest a person’s previous infection status and timing should be considered alongside their booster vaccinations to predict protection. However, this may be difficult to implement as infection surveillance has decreased in most countries compared with earlier in the pandemic. In any case, <a href="https://commission.europa.eu/strategy-and-policy/coronavirus-response/safe-covid-19-vaccines-europeans/eu-digital-covid-certificate_en">COVID certificates</a> are used less commonly now.</p>
<p>They also suggest their findings could be used to inform the optimal timing for booster vaccination strategies. That is, there’s probably merit in waiting some time after an infection before getting a booster.</p>
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Read more:
<a href="https://theconversation.com/covid-reinfections-could-be-more-severe-for-some-but-overall-evidence-doesnt-give-us-cause-for-concern-185732">COVID reinfections could be more severe for some – but overall evidence doesn't give us cause for concern</a>
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<p>Further high quality, long-term follow up studies will be important to supplement these findings, as the authors acknowledge there are not as many studies on natural infection compared with protection after vaccination. There were also few studies mapping protection against newer omicron sublineages. As the pandemic continues, there remains much to learn about immune protection against this evolving virus.</p><img src="https://counter.theconversation.com/content/200044/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Zania Stamataki receives funding from the Medical Research Foundation and Innovate UK. She collaborates with AstraZeneca on projects unrelated to topics in this article. </span></em></p>Previous infection was highly protective against reinfection with alpha, beta and delta variants, but less so against omicron BA.1.Zania Stamataki, Associate Professor in Viral Immunology, University of BirminghamLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1981082023-02-09T12:56:34Z2023-02-09T12:56:34ZGenetics might explain why some people have never had COVID – but we shouldn’t be too focused on finding out<figure><img src="https://images.theconversation.com/files/508366/original/file-20230206-29-p6o6gc.jpg?ixlib=rb-1.1.0&rect=6%2C0%2C4486%2C3003&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/portrait-brunette-man-surgical-bandage-on-1650865489">LL_studio/Shutterstock</a></span></figcaption></figure><p>It’s been over three years since the first known COVID infection. Since then, we’ve seen <a href="https://www.worldometers.info/coronavirus/">hundreds of millions</a> of cases around the globe. </p>
<p>You’ve probably had it – at least once, if not multiple times – as has nearly everyone you know. As continued waves of infections arrive, fewer and fewer people have never caught COVID. But, even taking into account those who have had it and not realised, there are probably still some people out there who have managed to avoid the virus altogether (so far).</p>
<p>Last year, I wrote about <a href="https://theconversation.com/havent-had-covid-yet-it-could-be-more-than-just-luck-181708">people who had yet to be infected</a>. Were they somehow immune? Did they possess some advantageous genetic mutation? Were they simply avoiding people and continuing to take precautions? Or had they just been lucky, and their time was inevitably going to come?</p>
<p>Unfortunately, we still don’t know why some people have managed to avoid COVID for so long. Science takes time. We saw research occur at unprecedented speed in 2020 to understand SARS-CoV-2 (the virus that causes COVID) and to develop treatments and vaccines. But that level of funding and collaboration is hard to sustain in a world with so many worthwhile areas of research.</p>
<p>That said, some research is looking in particular at whether a genetic element helps explain why certain people have never caught COVID. But while this research is important, we shouldn’t lose focus on those who are suffering from the disease and its longer-term effects.</p>
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Read more:
<a href="https://theconversation.com/havent-had-covid-yet-it-could-be-more-than-just-luck-181708">Haven't had COVID yet? It could be more than just luck</a>
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<h2>Is immunity in the genes?</h2>
<p>The <a href="https://www.covidhge.com/">COVID Human Genetic Effort</a>, led by researchers in the US, has recruited people with known exposure to the virus, but who haven’t had it themselves. This includes, for example, healthcare workers or people who lived in a household with a confirmed case of COVID.</p>
<p>Scientists will be examining their DNA and looking for unusual mutations that may explain an apparent resistance to SARS-CoV-2 infection. This may be a mutation in the cellular receptors or enzymes needed for the virus to gain entry to our cells, or perhaps a mutation in a gene involved in the immune response to infection.</p>
<p>Studies that look to uncover anomalies in our DNA, termed <a href="https://www.genome.gov/about-genomics/fact-sheets/Genome-Wide-Association-Studies-Fact-Sheet">genome-wide association studies</a>, have already been able to identify genetic mutations that make some people resistant to other infections like <a href="https://www.nature.com/articles/382722a0">HIV</a> and <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6466115/">norovirus</a> (the winter vomiting bug). If we can identify the reasons people may be immune to a particular virus then, theoretically, that knowledge could be used to prevent the infection. </p>
<p>But is it really that simple? Despite our understanding of the genetic mutations that protect a lucky minority of people against norovirus, there’s no vaccine or treatment for this virus. And the infamous “<a href="https://theconversation.com/worlds-first-gene-edited-babies-premature-dangerous-and-irresponsible-107642">CRISPR babies</a>” (several children born in 2018 whose genomes had been edited in an attempt to make them immune to HIV), received criticism for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6342697/">dubious ethics</a>, not to mention being illegal.</p>
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<img alt="An illustration of DNA." src="https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/508399/original/file-20230206-31-16bfgj.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Genetic mutations might explain why some people have never caught COVID.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/science-biotechnology-dna-illustration-abstract-1440959093">Billion Photos/Shutterstock</a></span>
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<p>It’s possible that it’s not a mutation in one gene, but a combination of mutations in multiple genes, that render a small number of people immune to COVID. Targeting multiple genes without causing any unwanted side-effects can be tricky and would make it much harder to harness this knowledge for anti-COVID drugs. </p>
<p>But understanding the genetic mutations that make someone resistant to COVID could provide valuable insight into how SARS-CoV-2 infects people and causes disease. In other words, it may be interesting scientifically, but perhaps not clinically. </p>
<p>While it will be some time before we have answers from these studies, scientists do believe there is a small group of people who are <a href="https://www.nytimes.com/2022/12/14/briefing/never-covid.html">naturally immune</a> to SARS-CoV-2 owing to their genes.</p>
<h2>Time to shift focus?</h2>
<p>As scientists, we can become fixated on certain details of our research. It’s always important to remind ourselves that there are people on the other end of these infectious diseases.</p>
<p>Although SARS-CoV-2 continues to infect people across the world, and is constantly mutating and evolving into new variants, its severity has in general been greatly reduced thanks to effective vaccines.</p>
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Read more:
<a href="https://theconversation.com/hybrid-immunity-a-combination-of-vaccination-and-prior-infection-probably-offers-the-best-protection-against-covid-183943">Hybrid immunity: a combination of vaccination and prior infection probably offers the best protection against COVID</a>
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<p>At the same time, an estimated two million people in the UK <a href="https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/prevalenceofongoingsymptomsfollowingcoronaviruscovid19infectionintheuk/2february2023">report long COVID</a>, of which nearly one-fifth have symptoms so severe the condition significantly limits their day-to-day activities. </p>
<p>While there are a few theories as to what contributes to long COVID, including <a href="https://www.nature.com/articles/d41586-022-02286-7">microclots in the blood</a> and chronic inflammation, we don’t really know why some people are affected and others are not. So perhaps our focus should shift from the genetic determinants of immunity to SARS-CoV-2 to exploring whether some people may have a genetic predisposition to a potentially life-altering chronic disease.</p><img src="https://counter.theconversation.com/content/198108/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Lindsay Broadbent has previously received funding from The Wellcome Trust. She is a member of The Microbiology Society.</span></em></p>Scientists are trying to find out whether there’s a genetic reason certain people have managed to avoid COVID for three years.Lindsay Broadbent, Lecturer in Virology, University of SurreyLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1972532023-01-20T06:14:05Z2023-01-20T06:14:05ZDoes COVID really damage your immune system and make you more vulnerable to infections? The evidence is lacking<figure><img src="https://images.theconversation.com/files/504486/original/file-20230113-21-anzeum.jpg?ixlib=rb-1.1.0&rect=49%2C0%2C5472%2C3596&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The northern hemisphere has seen a surge in winter viruses.</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/african-american-mother-measuring-sick-sons-2135037491">Drazen Zigic/Shutterstock</a></span></figcaption></figure><p>Over the past month or two, many <a href="https://fortune.com/well/2022/12/20/why-is-everyone-sick-now-holiday-winter-season-flu-covid-rsv-rising-cases-hospitalizations-tripledemic/">northern hemisphere countries</a> including the US and the UK have seen a large wave of respiratory viral infections. These include RSV (<a href="https://www.scientificamerican.com/article/rsv-is-surging-what-we-know-about-this-common-and-surprisingly-dangerous-virus/">respiratory syncytial virus</a>), flu and COVID in all ages, as well as bacterial infections such as <a href="https://theconversation.com/strep-a-three-doctors-explain-what-you-need-to-look-out-for-195972">strep A</a> in children. </p>
<p>Sometimes these infections can be very serious. The UK has seen a huge surge in hospital admissions during winter, putting the health service <a href="https://www.england.nhs.uk/2022/12/flu-pressure-rises-with-hospital-cases-up-seven-fold-in-a-month/">under further stress</a>. </p>
<p>This had led some to question whether COVID damages our immune systems, leaving those who have been infected more vulnerable to other infectious diseases like the flu. </p>
<p>Another idea put forward to explain the surge in respiratory viruses is that children “missed out” on common childhood infections during the height of the pandemic, and that this has left them more vulnerable to these infections now owing to an “immunity debt”. But how credible are these explanations?</p>
<h2>COVID and our immune systems</h2>
<p>The human immune system has evolved to deal with a host of different infections. It has a variety of weapons it can deploy which work together not only to eradicate infectious agents, but also to remember them for a more rapid and tailored response upon any subsequent encounter. </p>
<p>Likewise, many infectious agents have developed tricks to try to evade our immune system. For example, a parasite called <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2020.624178/full"><em>Schistosoma mansoni</em></a> disguises itself to avoid the immune system detecting it.</p>
<p>SARS-CoV-2, the virus that causes COVID-19, similarly has tricks up its sleeve. Like many other viruses, it’s been shown to <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9220273/">evade host immunity</a>, particularly <a href="https://www.biorxiv.org/content/10.1101/2023.01.03.522427v2">newer variants</a>. Recent studies showed it can interfere with immune cells’ ability to detect it <a href="https://www.pnas.org/doi/10.1073/pnas.2208525120">within cells</a>. This is concerning, but it’s not clear that such changes impact immunity to other infections.</p>
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<a href="https://theconversation.com/inflammation-the-key-factor-that-explains-vulnerability-to-severe-covid-144768">Inflammation: the key factor that explains vulnerability to severe COVID</a>
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<p>Short-lived changes in a person’s immune defences are normal when they’ve been exposed to an infection. Several studies have now shown that, in response to SARS-CoV-2, specialised white blood cells called lymphocytes grow in number. These lymphocytes also display changes in their features typical of cell <a href="https://www.science.org/doi/10.1126/sciimmunol.abd6160">activation</a>, such as changes in <a href="https://www.cell.com/cell/fulltext/S0092-8674(20)31008-4?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867420310084%3Fshowall%3Dtrue">surface proteins</a>.</p>
<p>Such changes may sound dramatic to the non-expert if taken out of context (called “ascertainment bias”). But they’re normal and merely indicate that the immune system is working as it should. Research has confirmed that, <a href="https://www.biorxiv.org/content/10.1101/2021.05.26.442666v3.full">for most people</a>, the immune system <a href="https://pubmed.ncbi.nlm.nih.gov/33821250/">regains balance</a> following recovery. </p>
<h2>Some exceptions</h2>
<p>SARS-CoV-2, like many viruses, doesn’t affect everyone equally. We’ve known for some time that certain groups, including older people and those with underlying health complications such as <a href="https://theconversation.com/inflammation-the-key-factor-that-explains-vulnerability-to-severe-covid-144768">diabetes or obesity</a>, can be more susceptible to severe disease when they contract COVID. </p>
<p>This vulnerability is associated with an irregular immune response to SARS-CoV-2 that results in inflammation. Here we see, for instance, reduced numbers of lymphocytes and changes to <a href="https://www.science.org/doi/10.1126/sciimmunol.abd2071">immune cells</a> known as <a href="https://www.science.org/doi/10.1126/sciimmunol.abd6197">phagocytes</a>.</p>
<p>Still, for most of these vulnerable people, the immune system <a href="https://pubmed.ncbi.nlm.nih.gov/33821250/">returns to normal</a> over the next two to four months. However, a small subset of patients, particularly those who had severe COVID or have underlying medical issues, retain <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2021.676932/full">some changes</a> beyond six months after infection.</p>
<p>The significance of these findings isn’t clear, and longer-term studies considering the impact of underlying health conditions on immune function will be needed. But for most people, there’s no evidence to suggest immune damage following a COVID infection.</p>
<figure class="align-center ">
<img alt="A man pricks his finger with blood sugar measuring device." src="https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/504489/original/file-20230113-26-72g8ug.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">For some people with underlying health conditions, immune changes appear to last longer.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/mature-man-checking-blood-sugar-level-1768028183">pikselstock/Shutterstock</a></span>
</figcaption>
</figure>
<h2>What about long COVID?</h2>
<p>Emerging <a href="https://www.medrxiv.org/content/10.1101/2022.08.09.22278592v1">evidence suggests</a> the most <a href="https://pubmed.ncbi.nlm.nih.gov/35027728/">marked and persistent</a> differences in immune cells after a COVID infection occur in people who have developed <a href="https://www.science.org/doi/10.1126/science.abm8108">long COVID</a>.</p>
<p>So far, no data points to immune deficiency in long COVID patients. But an overactive immune response can actually cause harm, and the immune cell changes seen in long COVID patients seem consistent with a vigorous immune response. This may explain the variety of post-infection consequences and symptoms that people with <a href="https://medicine.yale.edu/lab/iwasaki/projects/immunology-long-covid/">long COVID</a> face. </p>
<h2>Immunity debt</h2>
<p>The “immunity debt” hypothesis suggests the immune system is like a muscle requiring near-constant exposure to infectious agents to keep it functioning. So, the argument goes, a lack of exposure due to lockdowns damaged immune development, especially in children, by making our immune systems “forget” earlier knowledge. This supposedly left them more vulnerable to infections when social mixing returned to normal. </p>
<p>Though this idea has gained traction, there’s no immunological evidence to support it. It’s not true to say we require a constant background of infection for our immune system to work. Our immune systems are immensely robust and powerful. For example, immune memory to the 1918 influenza pandemic was still evident <a href="https://www.nature.com/articles/nature07231">after 90 years</a>. </p>
<p>It’s also not strictly true to say children weren’t exposed to viruses during the early pandemic. Lockdowns didn’t commence until after waves of the usual winter respiratory infections in 2019/2020, and schools in the UK reopened in autumn 2020 with variable preventive measures, so children were still exposed to infections, including COVID-19. </p>
<p>The cold-causing viruses didn’t completely vanish by any means. For example, there was a significant <a href="https://www.gov.uk/government/statistics/national-flu-and-covid-19-surveillance-reports-2021-to-2022-season">RSV outbreak</a> in the UK in 2021.</p>
<p>Nonetheless, lockdowns and other protective measures probably did reduce exposure to viruses, and for some children this shifted when and at what age they were first exposed to viruses such as RSV. This, taken alongside a high background of COVID, and relatively poor COVID and flu vaccine uptake, could all be making <a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1127554/Weekly_Flu_and_COVID-19_report_w1.pdf">this season</a> particularly bad. However, a change in the timing of when people are exposed leading to a surge of infections doesn’t necessarily mean that individual immunity has been damaged.</p>
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<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/covid-flu-rsv-how-this-triple-threat-of-respiratory-viruses-could-collide-this-winter-191822">COVID, flu, RSV – how this triple threat of respiratory viruses could collide this winter</a>
</strong>
</em>
</p>
<hr>
<p>Our knowledge of the immune response to COVID is rapidly expanding. The most consistent findings show <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(22)00152-0/fulltext">how well vaccines</a> are protecting us from the very worst effects of SARS-CoV-2 and that, post-vaccination, our immune system is working exactly as it should. </p>
<p>However, findings of altered immune signatures in some recovered patients and those with long COVID require further investigation.</p><img src="https://counter.theconversation.com/content/197253/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sheena Cruickshank is affiliated with Independent SAGE.</span></em></p>A couple of theories are popular for explaining why we’re currently seeing very high levels of respiratory viruses, but they’re not based in science.Sheena Cruickshank, Professor in Biomedical Sciences, University of ManchesterLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1942312022-12-16T19:21:22Z2022-12-16T19:21:22Z‘Vaccinating’ frogs may or may not protect them against a pandemic – but it does provide another option for conservation<figure><img src="https://images.theconversation.com/files/501430/original/file-20221215-22-xp9m5j.jpg?ixlib=rb-1.1.0&rect=0%2C0%2C1280%2C850&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">California red-legged frogs are threatened with extinction.</span> <span class="attribution"><a class="source" href="https://flic.kr/p/4KnwCD">KQED QUEST/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by-nc/4.0/">CC BY-NC</a></span></figcaption></figure><p>When the COVID-19 pandemic first emerged, many <a href="https://scholar.google.com/citations?user=qnBAFpMAAAAJ&hl=en">wildlife disease researchers like me</a> were not too surprised. Some were intrigued it hadn’t happened sooner; after all, it is our job to observe, describe and study pandemic dynamics in animals.</p>
<p>Amphibians, for example, have been undergoing a global panzootic – the animal version of a pandemic – for decades. In the late 1990s, researchers identified the <a href="https://www.amphibianark.org/the-crisis/chytrid-fungus/">amphibian chytrid fungus</a>, which causes the often-lethal disease <a href="https://doi.org/10.1073/pnas.95.15.9031">chytridiomycosis</a>, as the probable culprit behind frog and salamander declines and extinctions from <a href="https://www.nespthreatenedspecies.edu.au/news-and-media/media-releases/these-frogs-need-our-help-scientists-name-the-australian-frogs-at-greatest-risk-of-extinction-four-likely-already-lost">Australia</a> to <a href="https://www.americanscientist.org/article/lessons-of-the-lost">Central America</a> and elsewhere that began 10, 20 or even <a href="https://doi.org/10.1002/ece3.3468">30 years before</a>.</p>
<p>Scientists have found this pathogen on <a href="https://www.researchgate.net/publication/26645573_Fisher_MC_Garner_TWJ_Walker_SF_Global_emergence_of_Batrachochytrium_dendrobatidis_and_amphibian_Chytridiomycosis_in_space_time_and_host_Ann_Rev_Microbiol_63_291-310">every continent that amphibians inhabit</a>, and the extensive <a href="https://deepblue.lib.umich.edu/bitstream/handle/2027.42/94283/mec5710.pdf;jsessionid=4E641E9F7DC2CEBA5C05B6777315B37A?sequence=1">global amphibian trade</a> has likely spread highly lethal strains around the world. The amphibian chytrid fungus is widespread in some <a href="https://doi.org/10.1371/journal.pone.0222718">geographic regions</a>, and, like the virus that causes COVID-19, it can <a href="https://doi.org/10.1534/g3.115.021808">mutate rapidly</a> and take new forms that cause varying disease severity.</p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/WpOl_yc8n6Q?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">Many amphibians are disappearing around the world.</span></figcaption>
</figure>
<p><a href="https://www.gov.uk/guidance/species-reintroductions-and-other-conservation-translocations">Conservation translocation</a> is an increasingly popular way to recover species that have experienced extensive population declines. It involves moving organisms to reestablish populations that have gone extinct, supplement existing ones or establish new ones in areas where the species was not previously present. However, when the amphibian chytrid fungus is prevalent in the landscape, frogs are likely to get sick again, hampering the success of translocation.</p>
<p>To avoid the setbacks of disease, researchers are <a href="https://ucnrs.org/inoculating-frogs-against-an-amphibian-pandemic/">using a tool</a> often employed against human pandemics: <a href="https://www.kqed.org/science/959844/can-a-new-vaccine-stem-the-frog-apocalypse">inoculations akin to vaccines</a>.</p>
<p>In <a href="https://doi.org/10.1002/ecs2.4294">our recent study</a>, my research team and I inoculated threatened <a href="https://ecos.fws.gov/ecp/species/2891">California red-legged frogs</a> against chytrid fungus before translocation by exposing them to the chytrid fungus in the laboratory. We wanted to see if we could activate their immune systems and give them an advantage over the fungus once they are released. Our results were unexpected.</p>
<h2>Nothing a cocktail won’t cure</h2>
<p>Since 2017, Yosemite National Park has been actively translocating California red-legged frogs to <a href="https://www.nps.gov/yose/learn/news/threatened-california-red-legged-frogs-making-a-comeback-in-yosemite-national-park-after-a-50-year-absence.htm">Yosemite Valley</a>, where the chytrid fungus is already present. We used a <a href="https://doi.org/10.1002/ecs2.4294">small subset</a> of these translocated frogs in our study.</p>
<p>We collected wild frog eggs at a place where the species is thriving, about 100 miles northwest of Yosemite Valley, then raised them in captivity at the San Francisco Zoo. Once they metamorphosed into juvenile frogs, we bathed 20 in a “cocktail” of four live, active strains of the fungus. After three weeks, they were given a bath of an antifungal drug to halt the infection. Another 40 frogs that were not exposed to the fungus were also given a bath of an antifungal drug. </p>
<p>Then we reexposed the 20 previously infected frogs to the fungus a second time, while 20 previously uninfected frogs were exposed to the fungus for the first time. We wanted to see how frogs with a second infection – namely, those that were “vaccinated” – compared with those that were infected only once.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Scanning electron micrograph of chytrid fungus" src="https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=482&fit=crop&dpr=1 600w, https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=482&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=482&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=605&fit=crop&dpr=1 754w, https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=605&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/501438/original/file-20221215-15-uz70p9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=605&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 chytrid fungus has devastated frog populations globally.</span>
<span class="attribution"><a class="source" href="https://www.scienceimage.csiro.au/image/1392">Alex Hyatt/CSIRO</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>What we found was surprising: 35% of frogs infected only once successfully cleared the infection without vaccination or an antifungal drug. This suggested that they have some measure of <a href="https://www.ncbi.nlm.nih.gov/books/NBK26846/">innate immunity</a>, meaning their immune system’s first line of defense was able to fight off the fungus. In addition, frogs infected a second time had a 31% overall lower rate of infection than those that were infected only once. This suggested that the vaccinelike treatment also works by stimulating <a href="https://www.ncbi.nlm.nih.gov/books/NBK21070/">adaptive immunity</a>, meaning their immune system learned to recognize the fungus from their first exposure and fight it off more efficiently. None of the frogs died from their fungal infections.</p>
<p>Before releasing them to the wild, we treated the frogs with an antifungal drug and monitored to make sure they were disease-free. We attached tiny transmitters with beaded belts around their waists so we could track their infections and survival over three months.</p>
<p>Unexpectedly, we found no difference in disease burden between the frogs that had never been infected and those that had been previously infected in the laboratory. This suggests that immunizing this species for chytrid fungus, at least in Yosemite, may be unnecessary to ensure their survival after reintroduction.</p>
<p>Indeed, the California red-legged frogs released into Yosemite Valley are thriving three years after our experiment and six years after their first translocation. They are hibernating successfully through the cold winters and emerging early in the spring for reproduction.</p>
<h2>Hope for the future</h2>
<p>Our study takes a new approach to the emerging tool of inoculation against the chytrid fungus. By combining ex situ, or laboratory, experiments with in situ, or in the field, implementation, we put lab observations to the test in the real world. This type of work strengthens collaborations between wildlife managers and zoos, which are increasingly needed as the <a href="https://www.un.org/sustainabledevelopment/blog/2019/05/nature-decline-unprecedented-report/">biodiversity crisis accelerates</a>.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="California red-legged frog floating in grassy water" src="https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/501435/original/file-20221215-17-59fogl.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">Preservation efforts for the California red-legged frogs are in progress.</span>
<span class="attribution"><a class="source" href="https://flic.kr/p/aw8gBV">Greg Schechter/Flickr</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>Though California red-legged frogs in Yosemite Valley didn’t seem to need vaccinations, this doesn’t mean that other imperiled amphibian species around the world do not. Research on chytrid inoculations in other species have had mixed results, ranging from <a href="https://doi.org/10.1371/journal.pone.0093356">not improving survival</a> to <a href="https://pubmed.ncbi.nlm.nih.gov/25008531/">reducing infection burden</a> associated with increased survival. One of the primary challenges of this approach to conservation is that even if vaccination increases survival after initial release, this immunity does not carry forward to successive generations.</p>
<p>There is hope, however. Researchers are working to identify the <a href="https://doi.org/10.1111/acv.12459">genetic signatures associated with immunity</a> to the chytrid fungus. If successful, breeding programs can artificially select for – and perhaps even <a href="https://www.sciencedirect.com/science/article/pii/S0169534721003384">gene-edit</a> – protective traits to give frogs a leg up on a pathogen that has devastated amphibian populations worldwide.</p><img src="https://counter.theconversation.com/content/194231/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Andrea Adams previously received funding from the Yosemite Conservancy for conducting this research as a postdoctoral researcher at Yosemite National Park. Funding for her current academic appointment is received from the U.S. Fish and Wildlife Service.</span></em></p>Amphibians have been devastated by a chytrid fungus pandemic. Researchers immunized California red-legged frogs in Yosemite to give them a fighting chance at survival, with surprising results.Andrea J. Adams, Researcher in Ecology, University of California, Santa BarbaraLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1957182022-12-16T13:13:54Z2022-12-16T13:13:54Z1918 flu pandemic upended long-standing social inequalities – at least for a time, new study finds<figure><img src="https://images.theconversation.com/files/499388/original/file-20221206-16-lo9q7q.jpg?ixlib=rb-1.1.0&rect=0%2C220%2C3000%2C1742&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">In this November 1918 photo, a nurse tends to a patient in the influenza ward of the Walter Reed hospital in Bethesda, Md. </span> <span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/VirusOutbreak1918InfluenzaCOVID19/97d84472fcad44449444ae3b7cc5f539/photo?Query=1918%20flu&mediaType=photo&sortBy=&dateRange=Anytime&totalCount=91&currentItemNo=29">AP Photo/Harris & Ewing via Library of Congress</a></span></figcaption></figure><p><em>The <a href="https://theconversation.com/us/topics/research-brief-83231">Research Brief</a> is a short take about interesting academic work.</em> </p>
<h2>The big idea</h2>
<p>Racial disparities in <a href="https://doi.org/10.1215/00703370-10235825">influenza deaths shrunk by 74% in U.S. cities</a> during the <a href="https://www.cdc.gov/flu/pandemic-resources/1918-pandemic-h1n1.html">1918 flu pandemic</a> due to an odd coincidence of virus and history. That’s the key finding of our recently published study in the journal Demography. </p>
<p>This conclusion contradicts the <a href="https://tidsskriftet.no/2017/05/global-helse/social-inequality-forgotten-factor-pandemic-influenza-preparedness">common claim</a> that crises like pandemics <a href="https://doi.org/10.1073/pnas.2020685118">make social inequalities worse</a>. The 1918 influenza pandemic was a surprising exception. </p>
<p>Prior to the 1918 pandemic, Black people in the U.S. died of respiratory diseases <a href="https://doi.org/10.1007/s13524-019-00789-z">at vastly higher rates</a> than white people. But our study found that urban white people in their 20s and 30s were especially vulnerable to the 1918 virus, dying at rates that were up to 20 times higher than normal. While the death rates of Black people in urban settings also spiked during the 1918 pandemic, they did so by a much smaller rate than in white populations. On average, across all age groups, white mortality increased fivefold, while Black mortality increased threefold.</p>
<p>Overall, Black people <a href="https://doi.org/10.7326/M20-2223">still died at higher rates</a> than white people during the 1918 pandemic, but the ratio of Black-to-white mortality – a measure of racial inequality – <a href="https://doi.org/10.3390/ijerph16142487">shrank dramatically</a> compared with other time periods. So while 1918 was wildly deadly across the world, the death rate among urban white young adults in the U.S. was truly unprecedented.</p>
<p><iframe id="i69Ni" class="tc-infographic-datawrapper" src="https://datawrapper.dwcdn.net/i69Ni/2/" height="400px" width="100%" style="border: none" frameborder="0"></iframe></p>
<h2>Why it matters</h2>
<p>One anomalous feature of the pandemic is well known: It <a href="https://doi.org/10.1371/journal.pone.0069586">killed many young adults</a> alongside children and elderly people, who are traditionally at risk from flu viruses.</p>
<p>But the unusually small racial inequality in flu deaths in the U.S. in 1918 is a little-known puzzle that contrasts with modern pandemics <a href="https://doi.org/10.1073/pnas.2205813119">like COVID-19</a> <a href="https://doi.org/10.2105/AJPH.2009.170241">and HIV</a>, which have hit Black communities especially hard. It also contrasts with a global tendency for <a href="https://doi.org/10.1186/s13643-018-0931-2">poorer populations to be more likely</a> to die from the flu.</p>
<p>Our study considered several hypotheses to explain the surprising patterns in the U.S. during the 1918 pandemic. One such potential explanation was that policies like school closures especially benefited Black populations because of their higher risk of dying from the flu in nonpandemic years when such measures were absent.</p>
<p>But only one explanation fits our evidence: Urban white young adults in the U.S. were deeply vulnerable in 1918 because of the way their immune systems had been programmed during childhood in the late 19th century. This is because the first flu people encounter as children is special: <a href="https://doi.org/10.1126/science.aag1322">It teaches the immune system</a> how to respond to future flu infections. However, research shows that this so-called immunological imprinting <a href="https://doi.org/10.1016/j.jaut.2017.04.008">can be harmful</a> when the virus someone later encounters is very different from the virus their immune system has been trained against.</p>
<figure>
<iframe width="440" height="260" src="https://www.youtube.com/embed/U6Ccdk5wPvk?wmode=transparent&start=0" frameborder="0" allowfullscreen=""></iframe>
<figcaption><span class="caption">The 1918 flu pandemic killed at least 50 million people worldwide.</span></figcaption>
</figure>
<p>The last flu pandemic to hit U.S. cities before 1918 was a <a href="https://doi.org/10.1073/pnas.1000886107">devastating global pandemic</a> that began in 1889. Exposure to that virus would have taught children’s immune systems to expect <a href="https://doi.org/10.1073/pnas.1324197111">what was probably an H3N8 flu</a>. But the devastation in 1918 was caused by the world’s first H1N1 pandemic. The two strains belong to two different groups of influenza viruses, and immune protection from H3N8 would not have conferred protection against H1N1. </p>
<p>To the contrary: People whose first flu exposure occurred in the 1890s would have likely had a compromised immune response to the 1918 pandemic because their immune system produced the wrong kind of antibodies that <a href="https://doi.org/10.1038/s41467-021-23977-1">crowded out more effective ones</a>.</p>
<p>In <a href="https://doi.org/10.1371/journal.pone.0069586">2013</a> and <a href="https://doi.org/10.1073/pnas.1324197111">2014</a> studies, two groups of virologists and demographers proposed and tested the hypothesis that 1890s imprinting explains the unusually high mortality of young adults during the 1918 pandemic. We adapted their argument to explain unusually small racial disparities as well. </p>
<p>This hypothesis suggests that the pattern of Black and white deaths in 1918 revolves around a historical coincidence. Black young adults were more often spared this fateful imprinting because they spent their childhoods in rural areas. As a result, though they often lived in deep poverty, they did not encounter some of the respiratory diseases that were rampant in cities. So while they were vulnerable to 1918’s novel flu, they were less so than people whose immune systems were primed to meet a virus like the one that circulated in the 1890s. </p>
<h2>What still isn’t known</h2>
<p>Immunologists are only beginning to understand the exact mechanisms through which imprinting affects long-term immune responses. Recent studies about the <a href="https://doi.org/10.3390/v11020122">early 20th century</a> and the <a href="https://doi.org/10.1038/s41467-021-23977-1">COVID-19 pandemic</a> support the idea that imprinting can significantly affect immune responses later in life. We all carry in our bodies the memories of our past disease exposures. </p>
<p>Those exposures <a href="https://doi.org/10.1007/s13524-019-00789-z">changed radically</a> during the 20th century, and the full consequences for population immunity in the COVID-19 era remain to be unraveled.</p><img src="https://counter.theconversation.com/content/195718/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Elizabeth Wrigley-Field receives funding from the Minnesota Population Center, which is funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development (grant number P2C HD041023).</span></em></p><p class="fine-print"><em><span>Martin Eiermann 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>During the 1918 flu pandemic, white people died at similar rates to Black Americans, according to a new study – a very different pattern than what occurred during the COVID-19 pandemic.Elizabeth Wrigley-Field, Assistant Professor of Sociology, University of MinnesotaMartin Eiermann, Postdoctoral Fellow in Sociology, Duke UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1961792022-12-12T13:37:37Z2022-12-12T13:37:37ZChina’s loosened COVID-19 policies – following years of aggressive lockdowns and quarantines – have left the country vulnerable<figure><img src="https://images.theconversation.com/files/500103/original/file-20221209-29029-7l4vwf.jpg?ixlib=rb-1.1.0&rect=0%2C195%2C5202%2C3392&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The Chinese government has loosened restrictions designed to limit the spread of COVID-19.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/epidemic-control-workers-wear-ppe-as-they-walk-to-disinfect-news-photo/1447909402?phrase=china%20zero%20covid%20&adppopup=true">Kevin Frayer/Stringer via Getty Images</a></span></figcaption></figure><p>After nearly three years of aiming to eliminate <a href="https://www.theguardian.com/world/2022/nov/29/china-zero-covid-policy-explained-30-seconds-lockdowns-outbreaks">COVID-19 through</a> mass lockdowns, robust contact tracing programs and international travel bans, the Chinese government has announced it is rolling back the “zero-COVID” policies that helped <a href="https://go.gale.com/ps/i.do?id=GALE%7CA618606601&sid=googleScholar&v=2.1&it=r&linkaccess=abs&issn=00280836&p=HRCA&sw=w&userGroupName=mlin_oweb">suppress the spread of the coronavirus</a> in the country. The Chinese Communist Party <a href="https://www.nytimes.com/2022/12/07/world/asia/china-zero-covid-protests.html">announced these changes</a> on Dec. 7, 2022, as <a href="https://www.nytimes.com/interactive/2021/world/china-covid-cases.html">rates of COVID-19 are on the rise</a> in major cities, following <a href="https://www.nytimes.com/2022/12/07/world/asia/china-zero-covid-protests.html">protests</a> demanding the end of zero-COVID policies. </p>
<p>The situation in China stands in stark contrast to the trajectory of the pandemic in the U.S. SARS-CoV-2 emerged with a bang, but thanks to a strong vaccination effort and the fact that a large portion of U.S. residents have been infected with the coronavirus, COVID-19 cases seem to be reaching somewhat of a steady state and <a href="https://doi.org/10.1056/NEJMp2004361">normal life has mostly resumed</a>.</p>
<p>I am a <a href="https://scholar.google.com/citations?user=YCsTY4sAAAAJ&hl=en&oi=ao">medical anthropologist</a> who studies <a href="https://www.sup.org/books/title/?id=23706">public health trends in China</a> from an epidemiologic and social perspective. </p>
<p>After largely <a href="https://www.nytimes.com/2020/08/23/world/asia/china-coronavirus-normal-life.html">containing the coronavirus in 2020</a>, China began enforcing a strict <a href="https://www.nytimes.com/2022/01/21/world/asia/china-zero-covid-policy.html">zero-COVID policy</a> leading up to the Beijing Olympics in 2022. The result is that China has not followed the standard path of a pandemic where people slowly gain immunity through exposure or vaccination, allowing society to open up over time. Combined with <a href="https://doi.org/10.1136/bmj.n969">questions about the efficacy of China’s vaccines</a> and comparatively low vaccination rates, many public health experts think that China will be hit hard by the coronavirus as the country rapidly <a href="https://www.nytimes.com/2022/12/02/health/china-covid-lockdowns.html">lifts its zero-COVID policy</a>. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A health worker checking a traveller at a checkpoint." src="https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/500104/original/file-20221209-41828-65pkn0.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">After the coronavirus first emerged in late 2019, the Chinese government severely limited travel in the region of Wuhan.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/VirusOutbreakChina/5fffda0e9b8841e8923776fefe4a693b/photo?Query=china%20lockdowns%20wuhan&mediaType=photo&sortBy=&dateRange=Anytime&totalCount=261&currentItemNo=9">AP Photo/Ng Han Guan</a></span>
</figcaption>
</figure>
<h2>China’s initial reaction to COVID-19</h2>
<p>Public health campaigns and control of emerging disease in China are entirely reliant on and directed by the government, which promotes health both for the <a href="https://globalizationandhealth.biomedcentral.com/articles/10.1186/s12992-019-0486-6">good of the people and the nation</a>. When COVID-19 emerged, the Chinese government was quick to institute mask-wearing policies and testing regimens, and it <a href="https://www.cnbc.com/2020/04/08/coronavirus-china-ends-lockdown-of-wuhan-city-where-outbreak-started.html">locked down the city of Wuhan and the surrounding region</a> where the coronavirus originated. With only the aid of these <a href="https://doi.org/10.1016/S0140-6736(20)31278-2">nonpharmaceutical interventions</a>, the Chinese government was very successful in containing the spread of COVID-19 after the initial wave hit Wuhan. </p>
<p>From the time China started recording cases in late December 2019, until the government ended its initial period of lockdown in April 2020, <a href="https://www.cnbc.com/2020/04/08/coronavirus-china-ends-lockdown-of-wuhan-city-where-outbreak-started.html">the government documented </a> 82,000 cases of COVID-19 and just over 3,300 deaths. Though not officially called a zero-COVID policy at the time, the control measures were born out of a goal of <a href="https://doi.org/10.2471%2FBLT.20.254045">eliminating COVID-19</a> from the country. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="A line of people waiting to be swabbed for COVID-19." src="https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/500105/original/file-20221209-41225-k8glwk.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">In the months leading up to the 2022 Beijing Olympics, China began ramping up zero-COVID measures, including mandatory testing requirements.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/VirusOutbreakChina/f24fab8b8eae4ee4a90c714caadbf960/photo?Query=china%20zero%20covid&mediaType=photo&sortBy=&dateRange=Anytime&totalCount=796&currentItemNo=230">AP Photo/Mark Schiefelbein</a></span>
</figcaption>
</figure>
<h2>Ramping up zero-COVID</h2>
<p>Life returned to normal in China after the initial wave of COVID-19 ravaged Wuhan. For most of 2020 and the first half of 2021, Chinese people were <a href="https://www.theguardian.com/world/2022/nov/29/china-zero-covid-policy-explained-30-seconds-lockdowns-outbreaks">out and about</a> in shopping malls, restaurants and bars. </p>
<p>During this same period, the coronavirus was rampaging across the U.S, Europe and other regions of the world, leading many health experts to say that the lockdowns in China, though brutal, were <a href="https://go.gale.com/ps/i.do?id=GALE%7CA618606601&sid=googleScholar&v=2.1&it=r&linkaccess=abs&issn=00280836&p=HRCA&sw=w&userGroupName=mlin_oweb">successful</a>. Between May 2020 and August 2021, people in China saw COVID-19 as a <a href="https://www.newyorker.com/news/news-desk/what-chinese-people-think-of-their-governments-zero-covid-policy">distant threat</a> and supported the government’s actions. </p>
<p>The situation changed in August 2021 when the Chinese government officially adopted what it calls the “<a href="https://www.ijbs.com/v18p5314.htm">Dynamic zero-COVID</a>” strategy to combat the new delta variant. This strict prevention policy included provisions for mass lockdowns <a href="https://doi.org/10.1016/S2213-2600(22)00142-4">aimed at eliminating</a> the disease in a particular region, even if just a small number of cases were found. </p>
<p>China <a href="https://www.newsweek.com/omicron-march-beijing-strains-china-zero-covid-policy-before-2022-olympics-1667828">ramped up enforcement of the policy</a> as the 2022 Winter Olympics approached. A <a href="https://www.theguardian.com/world/2021/nov/02/china-locks-down-shanghai-disneyland-and-tests-34000-visitors-after-single-covid-case">single case</a> could trigger a massive lockdown where the government would severely limit people’s movement and enforce quarantines, as occurred several times in Shanghai Disney. In some instances, people were held in stores or office buildings for <a href="https://www.nytimes.com/2022/01/21/world/asia/china-zero-covid-policy.html">several days</a> after exposure to an infected person. </p>
<p>Summer and fall 2022 were relatively quiet, with only around 1,000 confirmed infections per day. But since early November 2022, COVID-19 cases in China <a href="https://www.nytimes.com/interactive/2021/world/china-covid-cases.html">have climbed steadily</a>, with more than <a href="https://www.nytimes.com/interactive/2021/world/china-covid-cases.html">35,000 new cases detected per day</a> in the first week of December. </p>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="Chinese president Xi Jinping with people in masks behind him." src="https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/500106/original/file-20221209-34427-s6fynh.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">Following a wave of protests in late November and early December, the Chinese Communist Party announced that it would roll back some of the strictest travel limitations and quarantine requirements.</span>
<span class="attribution"><a class="source" href="https://newsroom.ap.org/detail/VirusOutbreakChina/1ca47c62c5f94606bc1a2586088c1d71/photo?Query=xi%20jinping%20zero%20covid%20&mediaType=photo&sortBy=&dateRange=Anytime&totalCount=76&currentItemNo=47">Jack Taylor/Pool Photo via AP</a></span>
</figcaption>
</figure>
<h2>What happens next?</h2>
<p>As of early December, COVID-19 rates in China were still relatively <a href="https://www.nytimes.com/interactive/2021/us/covid-cases.html">low compared to many places, including the U.S.</a>. But China faces some unique challenges thanks to low levels of immunity in the population and a disease control strategy that prioritized nonpharmaceutical interventions like mask-wearing, social distancing and <a href="https://www.nytimes.com/2022/06/14/business/china-covid-testing.html">frequent testing over vaccine administration</a>.</p>
<p>To date, 90% of the population in China <a href="https://www.nytimes.com/interactive/2021/world/covid-vaccinations-tracker.html">has been vaccinated</a>. Older people have been more reluctant, though, and only <a href="https://www.cnbc.com/2022/11/29/china-says-covid-vaccination-rates-for-seniors-has-climbed-over-the-last-two-weeks.html">66% of those over 80</a> have received two doses of a vaccine. A further concern arises from studies indicating that China’s vaccines may <a href="https://doi.org/10.1136/bmj.n969">not be as effective as the mRNA vaccines</a> used in the West. So far, China has <a href="https://www.cnn.com/2021/12/13/china/china-western-mrna-vaccine-mic-intl-hnk/index.html">not been willing to import</a> and administer Western mRNA vaccines. </p>
<p>In addition to concerns over vaccination, the zero-COVID policy has, to a large extent, successfully suppressed the coronavirus in China. The result is that since most people have not been exposed to the virus, they have not had a chance to develop immunity. This has likely <a href="https://www.theatlantic.com/health/archive/2022/12/china-zero-covid-wave-immunity-vaccines/672375/?utm_source=substack&utm_medium=email">left the country very susceptible</a> to a large outbreak. </p>
<p>There is also a social dimension to the problems facing China today. <a href="https://www.cbsnews.com/news/china-lockdowns-zero-covid-policy/">Recurring lockdowns</a> over the past year have damaged the economy and lessened <a href="https://www.nytimes.com/2022/12/03/opinion/china-covid-protests.html?smid=nytcore-ios-share&referringSource=articleShare">peoples’ patience</a> with restrictive policies. Despite government efforts to <a href="https://www.theguardian.com/world/2022/nov/28/china-censors-maskless-crowd-footage-in-world-cup-broadcasts">limit access to outside information</a>, people in China are learning that most other countries are functioning normally. Maintaining stringent zero-COVID policies has become increasingly difficult, as they <a href="https://www.nytimes.com/2022/12/01/opinion/china-covid-protests.html">wear on a populace</a> that wants life to return to normal.</p>
<p>The Dec. 7 announcement to ease COVID-19 restrictions is a continuation of a trend a few weeks in the making, but has been seen by many as a <a href="https://www.nytimes.com/2022/12/07/world/asia/china-zero-covid-protests.html">response to the widespread protests</a>. Testing centers <a href="https://www.nytimes.com/2022/12/01/world/asia/china-covid-protests-restrictions.html?utm_source=substack&utm_medium=email">are closing</a> and infected people are now allowed to <a href="https://www.reuters.com/world/china/china-allow-some-positive-covid-19-cases-quarantine-home-sources-2022-12-01/?mc_cid=b8f3c7dbfb&mc_eid=d60d414cea&utm_source=substack&utm_medium=email">quarantine at home</a> for the first time since the pandemic began. The digital health passes, issued to people who tested negative through daily PCR tests, are <a href="https://www.washingtonpost.com/world/2022/12/07/china-covid-easing-restrictions/">also no longer required</a> to enter public places. </p>
<p>In much of the world, COVID-19 has followed that <a href="https://www.jstor.org/stable/20025233">natural trajectory</a> of a pandemic. The story is different in China. The relaxation of zero-COVID policies may bring China more in line with the rest of the world in terms of what the people there can do, but the virus also gets a chance to run its natural course now that government actions will not suppress the spread. It is likely that in the coming months, the Chinese people will face the pain and suffering that many other places experienced in 2020 and 2021.</p><img src="https://counter.theconversation.com/content/196179/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Elanah Uretsky 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>Strict lockdowns, quarantines and testing have prevented many people in China from catching COVID-19. With concerns over Chinese vaccine efficacy and uptake, China may be facing a looming COVID-19 surge.Elanah Uretsky, Associate Professor of International and Global Studies, Brandeis UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1938612022-11-10T19:01:19Z2022-11-10T19:01:19ZWhy haven’t I had COVID yet?<figure><img src="https://images.theconversation.com/files/494349/original/file-20221109-22-h9y26d.jpg?ixlib=rb-1.1.0&rect=16%2C24%2C5447%2C3612&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/africanamerican-woman-using-cotton-swab-while-2114963081">Shutterstock</a></span></figcaption></figure><p>Throughout the pandemic, Australia has <a href="https://covid19.who.int/region/wpro/country/au">recorded</a> 10.4 million cases of COVID-19, with the majority occurring this year. </p>
<p>This is without doubt an underestimate, as not everyone tests for COVID-19 or reports their positive results. </p>
<p>The <a href="https://www.ncirs.org.au/least-two-thirds-australians-including-children-and-adolescents-have-had-covid-19-two-national">latest survey</a> of donor blood looked at the proportion of people who had antibodies against SARS-CoV-2, the virus that causes COVID-19. It found at least two thirds of Australians have been infected.</p>
<p><div data-react-class="Tweet" data-react-props="{"tweetId":"1587898978682961920"}"></div></p>
<p>That leaves about a third of the population who are yet to have COVID. </p>
<p>I’m one such “NOVID” – despite multiple confirmed COVID-19 exposures during the pandemic, I’m yet to have symptoms and test positive. </p>
<p>So what do we know about NOVIDs? </p>
<h2>First, we might not actually be NOVIDs</h2>
<p>Some people claiming they’ve never had COVID-19 might be surprised to learn they have virus-targeting antibodies in their blood that could only have been generated by infection. </p>
<p>The reliance on home rapid antigen tests (RATs), which are less sensitive than PCR testing, will contribute to many people failing to definitively determine whether they have COVID-19. </p>
<p>Under <a href="https://www.tga.gov.au/products/covid-19/covid-19-tests/covid-19-rapid-antigen-self-tests-home-use/covid-19-rapid-antigen-self-tests-are-approved-australia">ideal testing conditions</a>, the best tests detect SARS-CoV-2 infection more than 95% of the time. However in the real world, the detection rate is lower.</p>
<p>If you have mild symptoms that don’t last long, you’re less likely to test repeatedly and may miss your window to get a positive result. So some COVID-19 cases will escape detection by RATs. </p>
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Read more:
<a href="https://theconversation.com/could-i-have-had-covid-and-not-realised-it-178630">Could I have had COVID and not realised it?</a>
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<p>At this point, it’s important to distinguish between being infected with SARS-CoV-2 and experiencing the illness (COVID-19) caused by this infection. You can be infected without experiencing COVID-19 symptoms – this is called asymptomatic infection. </p>
<p>It’s unclear what proportion of Omicron subvariant cases are asymptomatic. Early in the pandemic, one in six people infected were <a href="https://jammi.utpjournals.press/doi/full/10.3138/jammi-2020-0030">asymptomatic</a> and it could now be as high as <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2795246?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=081722">50% or more</a> with Omicron. </p>
<p>So, many NOVIDs will have been infected with SARS-CoV-2, generated antibodies to the virus, but did not experience or notice any COVID-19 symptoms at the time, did not test and have remained unaware of their infection status (and whether they were unknowingly <a href="https://www.sip-spp.pt/media/ab3fhmiy/johansson_2021_oi_201061_1612890816-17333.pdf">transmitting</a> the virus).</p>
<figure class="align-center ">
<img alt="People sit on a train, some wear masks, others don't" src="https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/494355/original/file-20221109-15-a4qjc0.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">People who don’t have symptoms can still transmit the virus.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/oBnAP0eHmdY">Unsplash/Nick Fewings</a></span>
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<h2>What role does the immune system play?</h2>
<p>Everyone’s immune system is different. How your immune system responds to a particular infection is affected by many factors including your genes, gender, age, diet, sleep patterns, stress levels, history of other infections and illnesses, medications, vaccination status, and level of virus exposure. </p>
<p>So are some people less likely to get COVID-19 because of the strength of their immune system?</p>
<p>The status of our immune system at any given moment will impact our susceptibility to disease. So it’s unsurprising the people most susceptible to severe COVID-19 are those with less effective immunity because they have chronic diseases, are immune-suppressed or elderly. </p>
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<strong>
Read more:
<a href="https://theconversation.com/your-immune-system-is-as-unique-as-your-fingerprint-new-study-168228">Your immune system is as unique as your fingerprint – new study</a>
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<p>The other key variable is the virus. SARS-CoV-2 continues to evolve with <a href="https://theconversation.com/from-centaurus-to-xbb-your-handy-guide-to-the-latest-covid-subvariants-and-why-some-are-more-worrying-than-others-192945">new Omicron subvariants</a> continuing to emerge. This will affect how the virus interacts with us and the relative impact of different factors affecting our immune protection and susceptibility. </p>
<p>SARS-CoV-2 has proven itself to be particularly adept at evolving to generate viral variants that can evade our established immune protection. In addition, our immune protection is not stable and will begin to wane after a couple of months if not boosted by vaccination or infection. </p>
<h2>Are my genes protecting me?</h2>
<p>Let’s consider something that is relatively stable: your genes. </p>
<p>Scientists looking for associations between specific genes and disease can undertake genome-wide association studies. The effect of individual genetic variations on disease risk is usually very small, so identifying them requires large numbers of people and factoring in other variables that make us all different.</p>
<figure class="align-center ">
<img alt="People wait in a queue" src="https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/494354/original/file-20221109-23-77qqxt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Scientists are investigating whether genes affect our susceptibility for diseases.</span>
<span class="attribution"><a class="source" href="https://unsplash.com/photos/R72P3yZyYJ8">Meizhi Lang/Unsplash</a></span>
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<p>In <a href="https://www.nature.com/articles/d41586-021-01773-7#:%7E:text=08%20July%202021-,Human%20genetic%20variants%20identified%20that%20affect%20COVID%20susceptibility%20and%20severity,risk%20of%20severe%20COVID%2D19.">once such study</a>, researchers compared genomes of nearly 50,000 people with COVID-19 with the genomes of 2 million people without known infection.</p>
<p>They identified regions in the genome (loci) associated with contracting COVID-19 and other genetic regions associated with disease severity. So this is evidence that, like many other diseases, certain genes do modify the risk of COVID-19. </p>
<p>While association is not causation, these types of genomic studies point us in a direction to better understand the biology of COVID-19 to address questions such as who might be at risk of severe disease or long COVID and assist development of new therapies to prevent these outcomes. </p>
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<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/do-genetic-differences-make-some-people-more-susceptible-to-covid-19-149303">Do genetic differences make some people more susceptible to COVID-19?</a>
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<p>Another <a href="https://www.nature.com/articles/s41590-021-01030-z?utm_medium=affiliate&utm_source=commission_junction&utm_campaign=CONR_PF018_ECOM_GL_PHSS_ALWYS_DEEPLINK&utm_content=textlink&utm_term=PID100104362&CJEVENT=2d2248685e3911ed838df31f0a1c0e12">study</a> identified a small number of critically ill COVID-19 patients with rare gene variants. These could be directly linked to defective antiviral immunity. </p>
<p>So for a very small number of people, it appears their genes make them more susceptible to COVID. But for the vast majority of people, the picture is far more complicated.</p>
<h2>Could I have immunity from previous infection with a similar virus?</h2>
<p>SARS-CoV-2 is not the only respiratory coronavirus that regularly infects humans. Four others – 229E, HKU-1, OC43 and NL63 – share some similarity with SARS-CoV-2. </p>
<p>Most adults would have been infected by these viruses multiple times throughout their life. This raises the <a href="https://www.nature.com/articles/s41586-021-04186-8?utm_medium=affiliate&utm_source=commission_junction&utm_campaign=CONR_PF018_ECOM_GL_PHSS_ALWYS_DEEPLINK&utm_content=textlink&utm_term=PID100104362&CJEVENT=835ff5a15e3911ed836a01320a1c0e0b">possibility</a> that immunity generated by lifetime and/or recent exposure to these other coronaviruses might generate immunity that provides some protection against SARS-CoV-2 infection and symptomatic COVID-19. </p>
<p>More research is needed to better understand this, but the existing evidence is compelling and it’s certainly plausible.</p>
<p>The bottom line is there are many reasons why people who socialise and inevitably interact with people with COVID-19 believe they’ve never had COVID themselves. For most NOVIDs, it has been a combination of vaccination, leveraging a healthy immune system, sensible decisions and luck that have kept them COVID-free thus far. </p>
<p>Of course, luck eventually runs out, so enjoy your NOVID status while you can.</p><img src="https://counter.theconversation.com/content/193861/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Nathan Bartlett 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>You might not know you’ve had it. Or perhaps your immune system or genes have given you a boost. Or maybe you’re just lucky.Nathan Bartlett, Associate Professor, School of Biomedical Sciences and Pharmacy, University of NewcastleLicensed as Creative Commons – attribution, no derivatives.