tag:theconversation.com,2011:/uk/topics/r0-number-81978/articlesR0 number – The Conversation2022-07-27T04:13:58Ztag:theconversation.com,2011:article/1868262022-07-27T04:13:58Z2022-07-27T04:13:58ZNew COVID variants may be more transmissible but that doesn’t mean the R0 – or basic reproduction number – has increased<p>During the pandemic we have all become familiar with a lot of epidemiological concepts. </p>
<p>One that was introduced to us early in 2020 is the “basic reproductive number”, or R0. This tells us about the intrinsic contagiousness of a virus, or its inherent capacity to be spread from one person to another in a particular population. </p>
<p>We also learned about the “effective reproductive number”, or Reff. This tells us about the rate at which a virus is actually spreading through that population.</p>
<p>With the emergence of BA.4/5, there has been some confusion around how these concepts help us to understand why one variant spreads faster than another. </p>
<p>Just because a variant spreads faster, it doesn’t necessarily mean it has a higher R0.</p>
<h2>What does the R0 actually tell us?</h2>
<p>R0 tells us about the number of secondary cases arising from a single case in a fully susceptible population. It describes the potential capacity of a pathogen (such as a virus) to spread, and is pathogen-specific. </p>
<p>Pathogens with higher R0 values have the potential to cause larger epidemics. For ancestral strains of SARS-CoV-2 (the virus that causes COVID), R0 was <a href="https://doi.org/10.1371/journal.pone.0242128">estimated to be around 3</a>. </p>
<p>R0 is also population-specific. It depends on the population’s behaviour at “baseline”, before the pandemic. For example, a densely populated city with lots of indoor venues in which people mix is likely to have a higher R0 for the same pathogen than a region with a sparse population and less mixing between groups.</p>
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Read more:
<a href="https://theconversation.com/r0-how-scientists-quantify-the-intensity-of-an-outbreak-like-coronavirus-and-predict-the-pandemics-spread-130777">R0: How scientists quantify the intensity of an outbreak like coronavirus and predict the pandemic's spread</a>
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<h2>What about the Reff?</h2>
<p>The Reff is the average number of new infections caused by an infected individual in the presence of public health measures, behavioural change, and population immunity (from previous infection and vaccination). </p>
<p>The Reff will therefore change over time.</p>
<p>It is a <a href="https://epiforecasts.io/">key indicator</a> of whether an epidemic is growing or shrinking. When the Reff is above 1, the epidemic is growing. If control measures, population immunity, or other factors can bring the Reff below 1, the epidemic is in decline.</p>
<p>Throughout the pandemic, the Reff has been routinely estimated for Australia and <a href="https://www.health.gov.au/resources/publications/australian-national-disease-surveillance-plan-for-covid-19">reported</a> to decision-makers.</p>
<h2>How do new variants out-compete existing ones?</h2>
<p>The COVID pandemic can be divided into several distinct eras, each defined by the emergence of a new variant: </p>
<ul>
<li>Alpha in late 2020</li>
<li>Delta in mid-2021</li>
<li>Omicron BA.1 in late 2021</li>
<li>Omicron BA.2 in early 2022</li>
<li>and now Omicron BA.4 and BA.5. </li>
</ul>
<p>Each of these variants was able to outcompete and replace the one before it.</p>
<p>If we observe that a hypothetical “variant A” is spreading through a population faster than “variant B”, we say that variant A has a “growth advantage” over variant B. </p>
<p>This growth advantage, if sustained, means variant A will replace variant B as the new dominant variant spreading in the population. </p>
<p>A variant can have a growth advantage and not actually be intrinsically more transmissible. In fact, the R0 of variant A may be higher, lower, or the same as variant B.</p>
<p>This is because the growth advantage of variant A, compared to variant B, may be driven by any combination of:</p>
<ol>
<li>a shorter generation time</li>
<li>increased intrinsic transmissibility (R0)</li>
<li>an increased level of “immune evasion”.</li>
</ol>
<p>Each of these drivers has a different impact on the future epidemic trajectory and implications for the effectiveness of control measures.</p>
<p><strong>Shorter generation time</strong></p>
<p>A shorter generation time means a shorter time, on average, between a person becoming infected and then infecting another person. The average number of new infections arising from each infected person is the same for both variants, but those infections happen more quickly for variant A. This will lead to a more rapid rise in cases of variant A, even when R0 is the same.</p>
<p><strong>Intrinsic transmissibility</strong></p>
<p>Increased intrinsic transmissibility refers to the situation where the R0 of variant A is higher than that of variant B. Multiple different biological changes to the virus, such as changes that increase the infectiousness of an infected person, may drive this.</p>
<p><strong>Immune evasion</strong></p>
<p>Immune evasion refers to how easily a variant infects people who have previously been infected and or vaccinated.</p>
<p>Variants with very high levels of immune evasion can spread quickly in highly immune populations because there are simply more people in the population who are able to be infected. But it doesn’t mean they are intrinsically more transmissible.</p>
<p>In fact, they may even have a reduced R0 and still have a growth advantage.</p>
<p><strong>Implications for Reff</strong></p>
<p>All three of these mechanisms can result in a growth advantage, but have different implications for the Reff of variant A compared to variant B.</p>
<p>An increase in intrinsic transmissibility or immune escape will lead to an increased Reff for variant A compared to variant B. However a shorter generation time can lead to a growth advantage without affecting the Reff. If variant A has only a shorter generation time, it will spread faster through the population than variant B.</p>
<h2>How has this played out in the COVID pandemic?</h2>
<p>Over the course of the COVID pandemic, several variants have emerged with considerable growth advantage over previous variants: Alpha, then Delta, Omicron BA.1 and BA.2, and most recently, Omicron BA.4 and BA.5. </p>
<p>The reasons for the growth advantage over previous variants have been driven by different factors.</p>
<p>Alpha’s growth advantage over ancestral strains was estimated to be due to higher intrinsic transmissibility. Scientists <a href="https://pubmed.ncbi.nlm.nih.gov/33658326/">estimated</a> the basic reproduction number (R0) of Alpha was 43–90% higher than for ancestral strains. </p>
<p>When Omicron BA.1 rapidly emerged in late 2021 in highly immune populations (including Australia, where most <a href="https://www.abc.net.au/news/2021-03-02/charting-australias-covid-vaccine-rollout/13197518">jurisdictions</a> had achieved more than 85% second-dose vaccine coverage in eligible groups), scientists immediately suspected <a href="https://twitter.com/trvrb/status/1466076797670363140">immune evasion was playing a role</a>.</p>
<p><a href="https://twitter.com/_nickgolding_/status/1468226234995773443?s=12">Analyses of emerging data</a> quantified the relative contribution of immune evasion and intrinsic transmissibility that could explain the rapid spread.</p>
<p>Most recently, we have seen the rapid rise of Omicron BA.4 and BA.5 globally. Emerging <a href="https://www.medrxiv.org/content/10.1101/2022.05.16.22275151v1">evidence</a> suggests <a href="https://www.biorxiv.org/content/10.1101/2022.05.26.493517v1">immune evasion</a> is, once again, likely a significant factor contributing to the <a href="https://www.medrxiv.org/content/10.1101/2022.04.29.22274477v1">transmission advantage</a> of BA.4 and BA.5 over previous Omicron variants.</p>
<p>This means we expect BA.4 and BA.5 to spread rapidly in Australia, despite our very high levels of vaccination coverage and lots of previous infection. </p>
<p>However, the R0 may not have <a href="https://theconversation.com/australia-is-heading-for-its-third-omicron-wave-heres-what-to-expect-from-ba-4-and-ba-5-185598">changed</a>. Even with the same intrinsic transmissibility, simply having more of the population being susceptible again, means the same R0 will end up translating to more infections. </p>
<h2>Not a simple calculation</h2>
<p>Throughout the pandemic, infectious disease epidemiologists have had to carefully evaluate the available data to estimate why a new variant has a growth advantage.</p>
<p>Others, including some scientists <a href="https://theconversation.com/australia-is-heading-for-its-third-omicron-wave-heres-what-to-expect-from-ba-4-and-ba-5-185598">on The Conversation</a>, have unfortunately simply assumed that the growth advantage is due to an increased intrinsic transmissibility.</p>
<p>They have done this by multiplying the R0 of an existing variant by how much faster a new variant is estimated to be spreading. Repeated application of this approach has resulted in an inflated R0 estimate for BA.4/5, <a href="https://theconversation.com/why-we-corrected-our-estimates-for-the-reproduction-number-of-two-covid-subvariants-187624">similar to that of measles</a>.</p>
<p>While this approach was <a href="https://pubmed.ncbi.nlm.nih.gov/33658326/">OK for Alpha</a>, because household studies showed that the variant spread more efficiently in previously unexposed populations, it was not appropriate once Omicron appeared.</p>
<p>None of these considerations are unique to COVID. For example, new influenza variants mostly arise due to <a href="https://www.antigenic-cartography.org">immune escape</a>, driving a growth advantage and replacement of the previously circulating strain.</p>
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Read more:
<a href="https://theconversation.com/australia-is-heading-for-its-third-omicron-wave-heres-what-to-expect-from-ba-4-and-ba-5-185598">Australia is heading for its third Omicron wave. Here's what to expect from BA.4 and BA.5</a>
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<h2>So what is the R0 of BA.4/5?</h2>
<p>With the emergence of each new variant, the task has become more challenging as the population’s infection history (whether you’ve been infected before, when and how many times) makes interpretation of the data more and more difficult.</p>
<p>And so it is now very difficult to estimate the R0 for BA.4/5.</p>
<p>It is certainly higher than for Alpha and Delta, with the <a href="https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/1005395/23_July_2021_Risk_assessment_for_SARS-CoV-2_variant_Delta.pdf">weight of evidence</a> indicating a value at least double that of the ancestral variant (3). That would make it around 6.</p>
<p>And it is likely higher still because Omicron BA.1 out-competed Delta due to both an <a href="https://twitter.com/_nickgolding_/status/1468226234995773443?s=12">increase in intrinsic transmissibility and immune escape</a>.</p>
<p>We don’t yet fully understand why BA.2 replaced BA.1, with both <a href="https://doi.org/10.1101/2022.01.28.22270044">intrinsic transmissibility and immune escape potentially contributing</a>. But we do know that immune evasion is sufficient to explain the observed growth advantage of BA.4/5 over BA.2.</p>
<p>Therefore, our current best estimate for the R0 for BA.4/5 is that it is likely similar to that for BA.2, but the actual value remains uncertain. It is likely in the range of 6-10.</p>
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<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/why-we-corrected-our-estimates-for-the-reproduction-number-of-two-covid-subvariants-187624">Why we corrected our estimates for the reproduction number of two COVID subvariants</a>
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<img src="https://counter.theconversation.com/content/186826/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Freya Shearer receives funding from the National Health and Medical Research Council, the Australian Government Departments of Health and Foreign Affairs and Trade, and NSW Health. </span></em></p><p class="fine-print"><em><span>Catherine Bennett receives funding from Medical Research Future Find and the National Health and Medical Research Council. Catherine is also on the scientific advisory committee for Impact Health Technology and ResApp Healthcare Pty Ltd, and was an independent expert on the AstraZeneca COVID Vaccine Advisory Committee in 2021.</span></em></p><p class="fine-print"><em><span>James McCaw receives funding from the Australian Government Departments of Health and Foreign Affairs and Trade, the Australian Research Council and the National Health and Medical Research Council. He is an invited expert member of the Communicable Disease Network of Australia and between January 2020 and May 2022 was an invited expert member of the Australian Health Protection Principal Committee.</span></em></p><p class="fine-print"><em><span>Nick Golding receives funding from Australian, NSW, and WA Government Departments of Health, the Australian Research Council and the National Health and Medical Research Council. </span></em></p><p class="fine-print"><em><span>Hassan Vally 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>Just because a variant spreads faster, it doesn’t necessarily mean it has a higher R0.Freya Shearer, Research Fellow, Epidemic Decision Support, The University of MelbourneCatherine Bennett, Chair in Epidemiology, Deakin UniversityHassan Vally, Associate Professor, Epidemiology, Deakin UniversityJames McCaw, Professor in Mathematical Biology, The University of MelbourneNick Golding, Honorary Research Fellow, Telethon Kids Institute, and Professor, Curtin School of Population Health, Curtin UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1876242022-07-25T06:08:27Z2022-07-25T06:08:27ZWhy we corrected our estimates for the reproduction number of two COVID subvariants<figure><img src="https://images.theconversation.com/files/475816/original/file-20220725-11-lids7f.png?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-vector/fade-dots-background-halftone-distressed-pattern-1244098558">Shutterstock</a></span></figcaption></figure><p>We published an article earlier this month that contained incorrect estimates for the basic reproduction number (R0) for COVID subvariants BA.4/BA.5 and BA.2. We have now corrected the error, but I wanted to take a minute to explain what went wrong and how we are addressing it.</p>
<p>The article – <a href="https://theconversation.com/australia-is-heading-for-its-third-omicron-wave-heres-what-to-expect-from-ba-4-and-ba-5-185598">Australia is heading for its third Omicron wave. Here’s
what to expect from BA.4 and BA.5</a> –
estimated that the basic reproduction number (or R0) of Omicron subvariant
BA.2 was about 13.3 and BA.4/5 was 18.6, which is similar to measles.</p>
<p>As a number of scientists, as well as a <a href="https://www.reuters.com/article/factcheck-omicron-reproduction-number-idUSL1N2YW1T0">Reuters fact
check</a>, have now pointed out, these estimates are likely to be incorrect. That’s because R0 only takes into account “intrinsic transmissibility”, whereas a key factor contributing to the growth of BA.4/5 is “immune escape” – the ability
of the subvariant to evade immunity from vaccination or previous infection.</p>
<p>We have <a href="https://theconversation.com/australia-is-heading-for-its-third-omicron-wave-heres-what-to-expect-from-ba-4-and-ba-5-185598">corrected the BA.4/5 article</a>. And because we have used this simple but incorrect calculation previously on The Conversation (that is, a previous variant’s R0 multiplied by how much more infectious a new subvariant is), we will go through other affected articles and correct where necessary.</p>
<p>The epidemiological concepts that lie behind this error are tricky to explain, so we’ve also <a href="https://theconversation.com/new-covid-variants-may-be-more-transmissible-but-that-doesnt-mean-the-r0-or-basic-reproduction-number-has-increased-186826">commissioned a fresh article</a> by experts in the field, explaining what R0
is (and isn’t).</p>
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<em>
<strong>
Read more:
<a href="https://theconversation.com/new-covid-variants-may-be-more-transmissible-but-that-doesnt-mean-the-r0-or-basic-reproduction-number-has-increased-186826">New COVID variants may be more transmissible but that doesn't mean the R0 – or basic reproduction number – has increased</a>
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<p>The Conversation exists to provide reliable information and when we identify errors we aim to correct them and be as transparent as possible about what went wrong and what we are doing about it.</p>
<p>Republishers of the article have been notified of the correction. Going forward, we won’t use simple calculations to estimate the R0.</p><img src="https://counter.theconversation.com/content/187624/count.gif" alt="The Conversation" width="1" height="1" />
We published an article earlier this month that contained incorrect estimates for the basic reproduction number (R0) for COVID subvariants BA.4/BA.5 and BA.2. We have now corrected the error, but I wanted…Fron Jackson-Webb, Deputy Editor and Senior Health EditorLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1655382021-09-28T20:13:20Z2021-09-28T20:13:20ZHow contagious is Delta? How long are you infectious? Is it more deadly? A quick guide to the latest science<figure><img src="https://images.theconversation.com/files/422542/original/file-20210922-23-68rivz.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/young-woman-face-mask-using-mobile-1685691625">Shutterstock</a></span></figcaption></figure><p>Delta was recognised as a SARS-CoV-2 <a href="https://www.cdc.gov/coronavirus/2019-ncov/variants/variant-info.html#anchor_1632154493691">variant of concern</a> in <a href="https://www.who.int/en/activities/tracking-SARS-CoV-2-variants/">May 2021</a> and has proved extremely difficult to control in unvaccinated populations. </p>
<p>Delta has managed to <a href="https://medicalxpress.com/news/2021-09-delta-overwhelming-covid-variants.html">out-compete</a> other variants, including Alpha. Variants are classified as “of concern” because they’re either more contagious than the original, cause more hospitalisations and deaths, or are better at evading vaccines and therapies. Or all of the above. </p>
<p>So how does Delta fare on these measures? And what have we learnt since Delta was first listed as a variant of concern?</p>
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<p>
<em>
<strong>
Read more:
<a href="https://theconversation.com/is-delta-defeating-us-heres-why-the-variant-makes-contact-tracing-so-much-harder-164780">Is Delta defeating us? Here's why the variant makes contact tracing so much harder</a>
</strong>
</em>
</p>
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<h2>How contagious is Delta?</h2>
<p>The R0 tells us how many other people, on average, one infected person will pass the virus on to. </p>
<p>Delta has an <a href="https://www.bbc.com/news/health-57431420">R0 of 5-8</a>, meaning one infected person passes it onto five to eight others, on average.</p>
<p>This compares with an R0 of 1.5-3 for the original strain. </p>
<p>So Delta is twice to five times as contagious as the virus that circulated in 2020. </p>
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<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=1023&fit=crop&dpr=1 600w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=1023&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=1023&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1285&fit=crop&dpr=1 754w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1285&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/423286/original/file-20210927-17-1pk7d7a.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1285&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<h2>What happens when you’re exposed to Delta?</h2>
<p>SARS-CoV-2 is the virus that causes COVID-19. SARS-CoV-2 is transmitted through droplets an infected person releases when they breathe, cough or sneeze. </p>
<p>In some circumstances, transmission also occurs when a person touches a contaminated object, then touches their face. </p>
<figure class="align-center ">
<img alt="Four Turkish men walk across an open town space." src="https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422547/original/file-20210922-27-v13dlg.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">One person infected with Delta infects, on average, five to eight others.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/turkey-03-20-2020-four-people-1678223533">Shutterstock</a></span>
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<p>Once SARS-CoV-2 enters your body – usually through your nose or mouth – it starts to replicate. </p>
<p>The period from exposure to the virus being detectable by a PCR test is called the <em>latent</em> period. For Delta, one study suggests this is an <a href="https://www.medrxiv.org/content/10.1101/2021.07.07.21260122v2">average of four days</a> (with a range of three to five days). </p>
<p>That’s two days faster than the original strain, which took roughly six days (with a range of five to eight days). </p>
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<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=761&fit=crop&dpr=1 600w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=761&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=761&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=957&fit=crop&dpr=1 754w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=957&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/423460/original/file-20210928-21-19maks8.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=957&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="attribution"><span class="source">The Conversation</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
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<p>The virus then continues to replicate. Although often there are no symptoms yet, the person has become infectious. </p>
<p>People with COVID-19 <a href="https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2783099">appear to be</a> most infectious two days before to three days after symptoms start, though it’s unclear whether this differs with Delta. </p>
<p>The time from virus exposure to symptoms is called the <em>incubation</em> period. But there is often a gap between when a person becomes infectious to others to when they show symptoms. </p>
<p>As the virus replicates, the viral load increases. For Delta, the viral load is up to <a href="https://www.nature.com/articles/d41586-021-01986-w">roughly 1,200 times higher</a> than the original strain.</p>
<p>With faster replication and higher viral loads it is easy to see why Delta is challenging contact tracers and spreading so rapidly.</p>
<h2>What are the possible complications?</h2>
<p>Like the original strain, the Delta variant can affect many of the body’s organs including the lungs, heart and kidneys. </p>
<p>Complications include blood clots, which at their most severe <a href="https://www.abc.net.au/news/2021-08-07/delta-variant-of-covid-19-causing-heart-problems-young-people/100352868">can result in strokes or heart attacks</a>. </p>
<p>Around 10-30% of people with COVID-19 will experience prolonged symptoms, known as <a href="https://theconversation.com/the-mystery-of-long-covid-up-to-1-in-3-people-who-catch-the-virus-suffer-for-months-heres-what-we-know-so-far-161174">long COVID</a>, which can last for months and cause significant impairment, including in people who were previously well.</p>
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<img alt="Woman in a mask waits in hospital waiting room." src="https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422545/original/file-20210922-17-1m6p5qa.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Even previously well people can get long COVID.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/coronavirus-hospital-covid-19-woman-medical-1721906755">Shutterstock</a></span>
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<p>Longer-lasting symptoms can include fatigue, shortness of breath, chest pain, heart palpitations, headaches, brain fog, muscle aches, sleep disturbance, depression and the loss of smell and taste.</p>
<h2>Is it more deadly?</h2>
<p>Evidence the Delta variant makes people sicker than the original virus is growing. </p>
<p>Preliminary studies from <a href="https://www.medrxiv.org/content/10.1101/2021.07.05.21260050v2">Canada</a> and <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3861566">Singapore</a> found people infected with Delta were more likely to require hospitalisation and were at greater risk of dying than those with the original virus. </p>
<p>In the Canadian study, Delta resulted in a 6.1% chance of hospitalisation and a 1.6% chance of ICU admission. This compared with other variants of concern which landed 5.4% of people in hospital and 1.2% in intensive care.</p>
<p>In the Singapore study, patients with Delta had a 49% chance of developing pneumonia and a 28% chance of needing extra oxygen. This compared with a 38% chance of developing pneumonia and 11% needing oxygen with the original strain. </p>
<p>Similarly, a published study from <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(21)01358-1/fulltext">Scotland</a> found Delta doubled the risk of hospitalisation compared to the Alpha variant. </p>
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<img alt="Older man with cold symptoms lays down, wrapped in a blanket, cradling his head, holding a tissue to his nose." src="https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=401&fit=crop&dpr=1 600w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=401&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=401&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/422541/original/file-20210922-5935-1eqsau.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
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<span class="caption">Emerging evidence suggests Delta is more likely to cause severe disease than the original strain.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/coronavirus-warning-old-people-senior-man-1505023982">Shutterstock</a></span>
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<h2>How do the vaccines stack up against Delta?</h2>
<p>So far, the <a href="https://www.medrxiv.org/content/10.1101/2021.08.06.21261707v1.full.pdf">data show</a> a complete course of the <a href="https://www.nejm.org/doi/full/10.1056/nejmoa2108891">Pfizer</a>, <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3777268">AstraZeneca</a> or <a href="https://www.medrxiv.org/content/10.1101/2021.08.06.21261707v1.full.pdf">Moderna</a> vaccine reduces your chance of severe disease (requiring hospitalisation) by more than 85%. </p>
<p>While protection is lower for Delta than the original strain, studies show good coverage for all vaccines after two doses. </p>
<h2>Can you still get COVID after being vaccinated?</h2>
<p>Yes. <a href="https://theconversation.com/why-are-we-seeing-more-covid-cases-in-fully-vaccinated-people-an-expert-explains-166741">Breakthrough</a> infection occurs when a vaccinated person tests positive for SARS-Cov-2, regardless of whether they have symptoms. </p>
<p>Breakthrough infection <a href="https://theconversation.com/what-is-a-breakthrough-infection-6-questions-answered-about-catching-covid-19-after-vaccination-164909">appears more common</a> with Delta than the original strains.</p>
<p>Most symptoms of breakthrough infection <a href="https://theconversation.com/yes-you-can-still-get-covid-after-being-vaccinated-but-youre-unlikely-to-get-as-sick-163870">are mild</a> and don’t last as long. </p>
<p>It’s <a href="https://www.bbc.com/news/health-52446965#:%7E:text=Researchers%20conclude%20reinfection%20is%20uncommon,have%20had%20antibodies%20or%20not.">also possible</a> to get COVID twice, though this isn’t common. </p>
<h2>How likely are you to die from COVID-19?</h2>
<p>In Australia, over the life of the pandemic, 1.4% of people with COVID-19 have died from it, compared with 1.6% in the United States and 1.8% in the United Kingdom. </p>
<p>Data from the United States <a href="https://www.cdc.gov/mmwr/volumes/70/wr/mm7037e1.htm?s_cid=mm7037e1_w#T1_down">shows</a> people who were vaccinated were ten times less likely than those who weren’t to die from the virus. </p>
<p>The Delta variant is currently proving to be a challenge to control on a global scale, but with full vaccination and maintaining our social distancing practices, we reduce the spread. </p>
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<a href="https://theconversation.com/why-is-delta-such-a-worry-its-more-infectious-probably-causes-more-severe-disease-and-challenges-our-vaccines-163579">Why is Delta such a worry? It's more infectious, probably causes more severe disease, and challenges our vaccines</a>
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<p class="fine-print"><em><span>Lara Herrero does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>Delta is more contagious and appears to be more deadly. And it’s more likely to land those infected in hospital and intensive care. Here’s what the latest evidence says about the dominant variant.Lara Herrero, Research Leader in Virology and Infectious Disease, Griffith UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1587332021-05-05T12:10:12Z2021-05-05T12:10:12ZWhere coronavirus variants emerge, surges follow – new research suggests how genomic surveillance can be an early warning system<figure><img src="https://images.theconversation.com/files/398759/original/file-20210504-19-16ael83.jpg?ixlib=rb-1.1.0&rect=80%2C0%2C4417%2C3090&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Sequencing the whole genome of patient virus samples lets scientists watch for new variants.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/an-employee-collects-a-sample-in-a-gemotest-lab-in-the-city-news-photo/1208719050">Sergei Malgavko/TASS via Getty Images</a></span></figcaption></figure><p>Genomic surveillance programs have let scientists track the coronavirus over the course of the pandemic. By testing patient samples, researchers are able to diagnose COVID-19. But they’re also able to use genetic changes in the virus to recreate its travel routes and identify the emergence of new viral variants.</p>
<p><a href="https://scholar.google.com/citations?user=jdNYfp4AAAAJ&hl=en&oi=sra">As</a> <a href="https://scholar.google.com/citations?user=_BegzMEAAAAJ&hl=en&oi=ao">microbiologists</a>, we examined how quickly the coronavirus genome has mutated during the pandemic and then <a href="https://doi.org/10.1038/s41598-021-86265-4">figured out how quickly these changes led to new cases</a> and rapid disease spread.</p>
<p>By connecting genetic change with the appearance of new clusters of disease, our research suggests how genome surveillance can provide a new early warning of what’s to come. Daily reports on how the virus is evolving could sound the alarm before case numbers explode.</p>
<h2>Mutations happen and can be tracked</h2>
<p>Starting around 2012, researchers began to develop genome sequencing as a way for public health experts <a href="https://doi.org/10.1128/genomeA.00594-17">to track infectious diseases</a>. Basically they are able to “read” an organism’s whole genetic code, the long list of A, C, G and T molecules that comprise the blueprints for the proteins that carry out the cell’s functions.</p>
<p>When pathogens infect a host, they reproduce themselves. Changes to the genetic code can happen at this point – like typos you might make copying down a page of text, substituting an A for a T in one spot, for instance. These changes are mutations. They provide new instructions to the next generation that can give them new capabilities – maybe they are better able to move between hosts, survive and initiate outbreaks or cause new symptoms.</p>
<p>Multiple versions of the same organism, but with variations in the genetic code, circulate during a disease outbreak. Depending on how successful they are at infecting new hosts and spreading, various versions can become more or less common.</p>
<p>Historically, public health labs tracked disease outbreaks by the name of the pathogen – SARS, salmonella, Ebola and so on. But as the speed and accuracy of genome sequencing increased, researchers realized that the same pathogen can be divided into many different subpopulations based on genetic variation.</p>
<p>These are the variants you hear about with regard to the coronavirus – the B.1.1.7 strain that first emerged in the U.K., the B.1.617 version that was identified in India, and the B.1.427 and B.1.429 variants that both originated in California. All are technically classified as the same SARS-CoV-2 virus, but they may have quite different features.</p>
<h2>Screening isn’t the same as sequencing</h2>
<p>When a person’s sample is tested for SARS-CoV-2, the lab uses <a href="https://my.clevelandclinic.org/health/diagnostics/21462-covid-19-and-pcr-testing">a technique called PCR</a> to identify whether certain coronavirus genes are present. This method is good for screening – diagnosing whether the person in fact has COVID-19 or not. It also provides important surveillance data about how many people have the coronavirus in a particular time and place.</p>
<p>But it doesn’t sequence the whole genome, which is made up of 30,000 nucleotides – those As, Gs, Cs and Ts. The PCR screening test just looks for one small stretch of the coronavirus’s genetic code – the gene related to the virus’s spike protein that helps it infect human cells. This technique won’t flag mutations happening in other parts of the genome because it’s not looking for them.</p>
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<a href="https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="diagram of how scientists can use genetic sequence data from coronavirus" src="https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/398925/original/file-20210505-17-1yqzzhp.png?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>
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<span class="caption">Sequencing the genetic material of the coronavirus can help researchers trace the travel routes of the virus, diagnose infected people and inform research into vaccines and therapeutics.</span>
<span class="attribution"><span class="source">Bart Weimer and Darwin Bandoy</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
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<p>Other mutations are definitely occurring, though. Sequencing the entire genomes of coronavirus samples creates a massive list of variants. Our work tackles this ever-changing list to show that not only do mutations in the spike gene lead to new outbreak clusters – additional mutations in other genes increase outbreaks, too.</p>
<h2>Connecting variants and outbreaks</h2>
<p>To figure out the role of these mutations, we directly linked the variants present at a certain time and place with the coronavirus’s <a href="https://theconversation.com/r0-how-scientists-quantify-the-intensity-of-an-outbreak-like-coronavirus-and-predict-the-pandemics-spread-130777">reproductive number, known as R for short</a>. R is a way to quantify the intensity of an infectious disease outbreak. It stands for how many additional people an infected person will spread the germ to.</p>
<p>But R doesn’t tell you what version of the viral genome was passed along. By directly linking R and the variant present, we were able to pinpoint the specific mutation that was emerging and increasing viral spread. We found that as new variants became more common, COVID-19 diagnoses surged. </p>
<p>By merging genomics with classical epidemiology, we created a tool that factors in rising variants and R to warn how quickly cases will spread and which variants are more likely to trigger new outbreaks.</p>
<p>To test this approach, we linked the SARS-CoV-2 genotype to the daily R during the first three months of the pandemic using 150 genomes. Our method predicted the near future of outbreaks in four different countries that each had various levels of mandated social interventions.</p>
<p>This preliminary evidence relied on a small number of genome sequences, but it was all the data available from the early stages of the pandemic. As the pandemic continues, <a href="https://doi.org/10.1038/d41586-021-01069-w">labs are sequencing thousands of genomes</a> across the globe weekly. We replicated our initial estimates using 20,000 genomes from the U.K. and arrived at the same observation – new variants led to more transmission, variants are continuing to expand and will continue to increase in prevalence as the pandemic continues.</p>
<p>By incorporating genome sequencing data with information about transmissibility, we created a kind of early warning system, allowing us to forecast spreading events. In the real world, advance warning like this could inform public health decisions about social interventions. People can prepare for predicted outbreaks. A bonus is that our model also would show when highly contagious variants are declining – providing solid evidence to support loosening restrictions to allow a return to normalcy.</p>
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<a href="https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="People walk past a COVID restrictions sign on a city street" src="https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/398760/original/file-20210504-20-1xmyzu2.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">Just as valuable as early warning, variant information could help officials know when it’s safer to lift restrictions.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/covid-19-marshals-walk-past-a-covid-19-road-sign-in-old-news-photo/1232427963">SOPA Images/LightRocket via Getty Images</a></span>
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<h2>Scanning the horizon for future threats</h2>
<p>We believe that public health is at the dawn of integrating genome sequencing with infectious disease tracking. We envision a reference library of pathogen genomes, representing the diversity of their many emerging variants. It could be a new tool for epidemiologists, a part of routine surveillance programs that can last beyond the current pandemic.</p>
<p>In the future, scientists hopefully won’t need to wait for an outbreak to grow. Our research suggests that by identifying a rise in variants early, public health officials can quickly respond – before the inevitable rise in new disease cases. We think this kind of early warning system can increase the public’s safety for any pathogen and reduce outbreaks for all types of organisms.</p>
<p>[<em>Over 100,000 readers rely on The Conversation’s newsletter to understand the world.</em> <a href="https://theconversation.com/us/newsletters/the-daily-3?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=100Ksignup">Sign up today</a>.]</p><img src="https://counter.theconversation.com/content/158733/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Bart C. Weimer receives funding from multiple federal agencies and foundations to support his academic research. </span></em></p><p class="fine-print"><em><span>Darwin Bandoy receives funding from Philippine California Advanced Research Institute and University of the Philippines for his PhD studies . </span></em></p>By merging genomics with classical epidemiology, researchers are able to predict new disease outbreaks based on which viral variants are on the rise.Bart C. Weimer, Professor of Population Health & Reproduction, University of California, DavisDarwin Bandoy, Ph.D. Student in Integrative Pathobiology, University of California, DavisLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1598212021-05-04T04:57:22Z2021-05-04T04:57:22ZWe may never achieve long-term global herd immunity for COVID. But if we’re all vaccinated, we’ll be safe from the worst<p>In early 2020, during the first thrashes of the pandemic, <a href="https://www.theguardian.com/commentisfree/2020/apr/17/herd-immunity-is-a-fatal-strategy-we-should-avoid-at-all-costs">we were all talking about herd immunity</a>.</p>
<p>At that stage, many commentators were arguing we should let COVID-19 rip through populations so we could get enough people immune to the virus that it would stop spreading. <a href="https://www.theguardian.com/commentisfree/2020/apr/17/herd-immunity-is-a-fatal-strategy-we-should-avoid-at-all-costs">As I argued at the time</a>, this was a terrible idea that would overwhelm hospitals and gravely sicken and kill many people.</p>
<p>Now we have safe and effective vaccines, we can aim to reach herd immunity in a much safer way. It’s certainly possible we’ll be able to reach and maintain local herd immunity in certain regions, states and countries. However the pandemic ends, it will involve this immunity to some extent.</p>
<p>But it’s still very uncertain whether long-term, global herd immunity is achievable. It’s quite likely the coronavirus could continue to spread even in places with high proportions of their populations vaccinated. It will probably never be eliminated.</p>
<p>However, if we’re all vaccinated, we’ll be largely safe from the worst ravages of the infection even if it does break out.</p>
<h2>What is herd immunity again? And what does it mean for us long-term?</h2>
<p>There are <a href="https://academic.oup.com/cid/article/52/7/911/299077">a few different definitions of herd immunity</a>. Nevertheless, they all deal with the “reproductive number” of a disease, known as the R number. This is the average number of people an infected person will pass a disease on to, at a certain point in time.</p>
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Read more:
<a href="https://theconversation.com/what-is-herd-immunity-and-how-many-people-need-to-be-vaccinated-to-protect-a-community-116355">What is herd immunity and how many people need to be vaccinated to protect a community?</a>
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<p>The R number depends on how infectious a disease is. Measles is often used as an example, because it’s one of the most infectious diseases. In a group of people among whom no one is immune to the disease, on average <a href="https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(17)30307-9/fulltext">one person will pass measles on to around 15 others</a>.</p>
<p>But as more people in the community become immune, either through vaccination or getting the disease and recovering, each infected person will pass on the infection to fewer and fewer others. Eventually, we reach a point at which the R number is below 1, and the disease starts to die out. The R number falling below 1 here is in a population where there are no social restrictions, so the disease starts to die out because of immunity and not because of measures like lockdowns. This is one definition of herd immunity.</p>
<p>However, another potential definition is that herd immunity is a state where enough people are immune in a population that a disease won’t spread at all. One of the more confusing parts of the pandemic is we scientists haven’t always used the <a href="https://academic.oup.com/cid/article/52/7/911/299077">same definition across the board</a>.</p>
<p>For example, when we say “reached the herd immunity threshold”, we could be talking about a transient state where we’re likely to see another epidemic in the near future, or a situation where the vast majority of a population is immune and thus the disease won’t spread at all. Both are technically “herd immunity”, but they’re very different ideas.</p>
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<h2>How’s herd immunity calculated?</h2>
<p>COVID-19 has an R number <a href="https://www.cdc.gov/coronavirus/2019-ncov/hcp/planning-scenarios.html">somewhere between 2 and 4</a> in groups of people where no one is immune. Using a <a href="https://gidmk.medium.com/herd-immunity-is-pretty-cool-adbc52630f9f">simple mathematical formula</a>, 50-75% of people need to be immune to COVID-19 for the R number to fall below 1 so it starts to die out, in a population with no social restrictions. Some researchers have done more complex versions of this calculation throughout the pandemic, but that’s the basic idea behind them all.</p>
<p>However, herd immunity is a moving target. For example, if everyone in your local population is taking great care to socially distance, COVID-19 won’t spread as much. Therefore, in practice, <a href="https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1008031#sec003">different cultures spread diseases to different extents</a>, so the R number varies in both place and time.</p>
<h2>Vaccines are the ultimate path to long-term immunity</h2>
<p>Vaccines give us immunity against diseases, often to a greater extent than contracting the disease itself, and without the <a href="https://www.sciencedirect.com/science/article/pii/S1201971220321809">nasty consequences</a> <a href="https://link.springer.com/article/10.1007%2Fs10654-020-00698-1">of being sick</a>.</p>
<p>Our COVID-19 vaccines are safe and effective. Without going too much into the debate over which one is better, they are all capable of getting us to a point at which the disease would no longer spread through the community. For some vaccines, the percentage of people who we need to immunise <a href="https://theconversation.com/herd-immunity-is-the-end-game-for-the-pandemic-but-the-astrazeneca-vaccine-wont-get-us-there-155115">is higher</a>. But it’s the same basic idea regardless, and we need to vaccinate as many people as we can to have a shot at herd immunity.</p>
<p>We can already see this happening in some places. For example, in the United Kingdom and Israel, enough people have been vaccinated that even though restrictions are being relaxed, infection rates are <a href="https://www.bbc.com/news/health-56722186">staying low or continuing to drop</a>. This is a beautiful sight.</p>
<h2>The coronavirus will probably never be eliminated</h2>
<p>Even with great vaccines, the problem is complex. There are almost always communities who aren’t immunised, for various reasons, even in countries with large proportions of the total population vaccinated. These small communities can continue to get sick and spread the disease long after the general population has passed the herd immunity line, which means there may always be some risk of COVID-19 outbreaks.</p>
<p>On top of this, new <a href="https://investors.modernatx.com/news-releases/news-release-details/moderna-announces-it-has-shipped-variant-specific-vaccine">variants</a> of the virus have emerged. Our current vaccines are <a href="https://elemental.medium.com/will-we-need-covid-19-booster-shots-heres-the-lowdown-cc64e64c6d03">probably enough</a> to provide most people with immunity to the original strain in the long term. But several variants may <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa2102214">substantially reduce our vaccines’ effectiveness</a> as time goes by, so we may need boosters at some point.</p>
<p>What’s more, the global situation isn’t rosy. India and Brazil are <a href="https://www.theguardian.com/news/2021/apr/28/crime-against-humanity-arundhati-roy-india-covid-catastrophe">currently experiencing</a> horrifying COVID-19 outbreaks. The global case count continues to rise, partially because developed nations have hoarded vaccine doses jealously, despite this being a <a href="https://theconversation.com/3-ways-to-vaccinate-the-world-and-make-sure-everyone-benefits-rich-and-poor-155943">terrible approach to a pandemic</a>. Rising case numbers anywhere increase the chances even more variants pop up, thereby impacting us all.</p>
<p>Even if we overcome vaccine hesitancy and global inaction, and we immunise most of the world, we may not be protected against the virus forever. Even higher-income nations <a href="https://time.com/5942246/eliminate-covid-19-u-s/">may never get rid of COVID-19</a>.</p>
<p>It’s quite likely this virus will never be eradicated (eliminated from every country across the globe). There may be places where the disease is gone, where local campaigns are successful, but there’ll also be places where the disease is still spreading.</p>
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Read more:
<a href="https://theconversation.com/covid-19-will-probably-become-endemic-heres-what-that-means-146435">COVID-19 will probably become endemic – here's what that means</a>
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<h2>What does this mean for Australia?</h2>
<p>This presents a challenge for Australia. We have virtually no local COVID-19 transmission, so there’s no real risk from the virus as long as our border controls hold steady.</p>
<p>However, we probably can’t maintain this level of vigilance forever. And even with our very effective vaccines, we may not have long-term herd immunity — of any definition — to COVID-19. </p>
<p>At some point in the future, it’s likely we will see some cases of COVID-19 spreading in even the safest places in the world, including Australia.</p>
<p>Even so, getting vaccinated <a href="https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3789264">enormously reduces</a> your risk of severe outcomes like hospitalisation and death. We should aim to vaccinate as many people as possible, while acknowledging that the future is inherently uncertain, and herd immunity is a challenging goal.</p><img src="https://counter.theconversation.com/content/159821/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Gideon Meyerowitz-Katz 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>It’s quite likely this virus will never be eliminated from the world. But even so, getting vaccinated enormously reduces your risk of severe outcomes like hospitalisation and death.Gideon Meyerowitz-Katz, PhD Student/Epidemiologist, University of WollongongLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1399502020-06-05T12:06:21Z2020-06-05T12:06:21ZA few superspreaders transmit the majority of coronavirus cases<figure><img src="https://images.theconversation.com/files/339938/original/file-20200604-67399-131jhv5.jpg?ixlib=rb-1.1.0&rect=218%2C223%2C3323%2C2392&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">A few people in the crowd will be responsible for the bulk of a disease’s spread.</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/commuters-wearing-protective-masks-wait-for-a-train-at-the-news-photo/1215807811">Pacific Press /LightRocket via Getty Images</a></span></figcaption></figure><p><em>The coronavirus has traveled the globe, infecting one person at a time. Some sick people might not spread the virus much further, but some people infected with the SARS-CoV-2 are what epidemiologists call “superspreaders.”</em> </p>
<p><em><a href="https://scholar.google.com/citations?user=k4UBB88AAAAJ&hl=en&oi=ao">Elizabeth McGraw</a>, the director of the <a href="https://www.huck.psu.edu/institutes-and-centers/center-for-infectious-disease-dynamics">Center for Infectious Disease Dynamics</a> at Pennsylvania State University, explains the evidence and why superspreaders can be crucial to a disease’s transmission.</em></p>
<h2>What is a superspreader?</h2>
<p>Early in the outbreak, researchers estimated that a person carrying SARS-CoV-2
would, on average, <a href="https://www.imperial.ac.uk/mrc-global-infectious-disease-analysis/news--wuhan-coronavirus/">infect another two to three people</a>. More recent studies have argued, however, that this number <a href="https://www.harvardmagazine.com/2020/05/r-nought">may actually be higher</a>.</p>
<p>As early as January, though, there were reports out of Wuhan, China, of a single patient who <a href="https://www.cnn.com/2020/01/23/health/wuhan-virus-super-spreader/index.html">infected 14 health care workers</a>. That qualifies him as a super spreader: someone who is responsible for infecting an especially large number of other people.</p>
<p>Since then, epidemiologists have tracked a number of other instances of SARS-CoV-2 superspreading. In South Korea, around <a href="https://www.livescience.com/coronavirus-superspreader-south-korea-church.html">40 people who attended a single church service</a> were infected at the same time. At a choir practice of 61 people in Washington state, <a href="https://www.cdc.gov/mmwr/volumes/69/wr/mm6919e6.htm">32 attendees contracted confirmed COVID-19</a> and 20 more came down with probable cases. In Chicago, before social distancing was in place, one person that attended a dinner, a funeral and then a birthday party was <a href="https://chicago.suntimes.com/politics/2020/4/8/21214375/super-spreader-coronavirus-spread-chicago-patients-deaths-cdc-covid-19">responsible for 15 new infections</a>.</p>
<p>During any disease outbreak, epidemiologists want to quickly figure out whether superspreaders are part of the picture. Their existence can accelerate the rate of new infections or substantially expand the geographic distribution of the disease.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/312664/original/file-20200129-92959-m1ltr9.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">A connected world of international travelers sets the stage for geographic superspreading.</span>
<span class="attribution"><a class="source" href="https://www.shutterstock.com/image-photo/contrail-dark-blue-sky-beautiful-show-9683023">aleksander hunta/Shutterstock.com</a></span>
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<h2>What are the characteristics of a superspreader?</h2>
<p>Whether someone is a superspreader or not will depend on some combination of the pathogen, the patient’s biology and their environment or behavior.</p>
<p>Some infected individuals might shed more virus into the environment than others if their immune system has trouble subduing the invader. Additionally, <a href="https://theconversation.com/infected-with-the-coronavirus-but-not-showing-symptoms-a-physician-answers-5-questions-about-asymptomatic-covid-19-137029">asymptomatic individuals</a> – <a href="https://www.cnn.com/2020/04/01/europe/iceland-testing-coronavirus-intl/index.html">up to 50% of all those who get COVID-19</a> – will continue their normal activities, inadvertently infecting more people. Even people who ultimately do show symptoms are capable of <a href="https://doi.org/10.1038/s41591-020-0869-5">transmitting the virus during a pre-symptomatic phase</a>. </p>
<p>A person’s behaviors, travel patterns and degree of contact with others can also contribute to superspreading. An infected shopkeeper might come in contact with a large number of people and goods each day. An international business traveler may crisscross the globe in a short period of time. A sick health care worker might come in contact with large numbers of people who are especially susceptible, given the presence of other underlying illnesses.</p>
<p>Public protests – where it’s challenging to keep social distance and people might be raising their voices or coughing from tear gas – are <a href="https://theconversation.com/how-to-protest-during-a-pandemic-and-still-keep-everyone-safe-from-coronavirus-6-questions-answered-139978">conducive to superspreading</a>.</p>
<h2>How big a part of COVID-19 are superspreaders?</h2>
<p>Several recent preprint studies, which haven’t yet been peer-reviewed, have shed light on the role of superspreading in COVID-19’s dispersion around the globe.</p>
<p>Researchers in Hong Kong examined a number of disease clusters by using contact tracing to track down everyone with whom individual COVID-19 patients had interacted. In the process, they identified multiple situations where a single person was responsible for as many as six or eight new infections. </p>
<p>The researchers estimated that only 20% of all those infected with SARS-CoV-2 were <a href="https://doi.org/10.21203/rs.3.rs-29548/v1">responsible for 80% of all local transmission</a>. Importantly, they also showed that these transmission events were associated with people who had more social contacts – beyond just family members – highlighting the need to rapidly isolate people as soon as they test positive or show symptoms. </p>
<p>Another study by researchers in Israel took a different approach. They compared the genetic sequences of coronavirus samples from patients inside the country to those from other places. Based on <a href="https://theconversation.com/the-coronavirus-genome-is-like-a-shipping-label-that-lets-epidemiologists-track-where-its-been-136826">how different the genomes were</a>, they could identify each time SARS-CoV-2 entered Israel and then follow how it spread domestically.</p>
<p>These scientists estimated that <a href="https://doi.org/10.1101/2020.05.21.20104521">80% of community transmission events</a> – one person spreading the coronavirus to another – could be tracked back to just 1-10% of sick individuals.</p>
<p>And when another research group modeled the variation in how many other SARS-CoV-2 infections a single infected person tends to cause, they also found there were occasionally individuals who were very infectious. These people <a href="https://doi.org/10.12688/wellcomeopenres.15842.1">accounted for over 80% of transmissions</a> in a population.</p>
<h2>When have superspreaders played a key role in an outbreak?</h2>
<figure class="align-right zoomable">
<a href="https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=636&fit=crop&dpr=1 600w, https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=636&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=636&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=800&fit=crop&dpr=1 754w, https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=800&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/312638/original/file-20200129-92964-kxqly8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=800&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">Officials quarantined ‘Typhoid’ Mary Mallon in a hospital.</span>
<span class="attribution"><a class="source" href="https://commons.wikimedia.org/wiki/File:Mary_Mallon_in_hospital.jpg">Wikimedia Commons</a></span>
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<p>There are a number of historical examples of superspreaders. The most famous is <a href="https://www.history.com/news/10-things-you-may-not-know-about-typhoid-mary">Typhoid Mary</a>, who in the early 20th century purportedly infected 51 people with typhoid through the food she prepared as a cook.</p>
<p>During the last two decades, superspreaders have started a number of measles outbreaks in the United States. Sick, unvaccinated individuals visited densely crowded places like schools, hospitals, airplanes and theme parks where they <a href="https://doi.org/10.1001/jamapediatrics.2019.4357">infected many others</a>.</p>
<p>Superspreaders have also played a key role in the outbreaks of other coronaviruses, <a href="http://www.taipeitimes.com/News/world/archives/2004/02/23/2003099824/1">including SARS in 2003</a> and <a href="https://doi.org/10.3947/ic.2016.48.2.147">MERS in 2015</a>. For both SARS and MERS, superspreading <a href="https://doi.org/10.1186/s12916-015-0450-0">mainly occurred in hospitals</a>, with <a href="http://www.cidrap.umn.edu/news-perspective/2016/07/patient-proximity-key-korean-mers-super-spreader-event">scores of people being infected at a time</a>.</p>
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<a href="https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/312662/original/file-20200129-92959-4qx7wt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
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<span class="caption">Public health officials work to get the word out on how to protect yourself during an outbreak.</span>
<span class="attribution"><a class="source" href="http://www.apimages.com/metadata/Index/South-Korea-China-Outbreak/9250d36b1f274996a9eb600a4af27dc7/1/0">AP Photo/Ahn Young-joon</a></span>
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<h2>Can superspreading occur in all infectious diseases?</h2>
<p>Yes. Researchers have identified superspreaders in outbreaks of diseases caused by bacteria, <a href="https://doi.org/10.1186/s12879-019-3870-1">such as tuberculosis</a>, as well as those caused by viruses, <a href="https://doi.org/10.1038/nature04153">including measles</a> and <a href="https://www.eurekalert.org/pub_releases/2017-02/osu-dw021017.php">Ebola</a>. Just as appears to be the case with the coronavirus, some scientists estimate that in an outbreak of any given pathogen, 20% of the population is usually responsible for <a href="https://doi.org/10.1038/438293a">causing over 80% of all cases of the disease</a>.</p>
<p>The good news is that <a href="https://www.cdc.gov/foodsafety/outbreaks/investigating-outbreaks/investigations/control.html">the right</a> <a href="https://www.who.int/csr/disease/ebola/training/infection-prevention/en/">control practices</a> <a href="https://www.who.int/csr/bioriskreduction/infection_control/publication/en/">specific to how</a> <a href="https://www.who.int/ith/2020-24-01-outbreak-of-Pneumonia-caused-by-new-coronavirus/en/">pathogens are transmitted</a> – hand-washing, masks, quarantine, vaccination, reducing social contacts and so on – can slow the transmission rate and halt a pandemic.</p>
<p><em>This is an updated version of <a href="https://theconversation.com/what-is-a-super-spreader-an-infectious-disease-expert-explains-130756">an article</a> originally published on Jan. 30, 2020.</em></p>
<p>[<em>Get facts about coronavirus and the latest research.</em> <a href="https://theconversation.com/us/newsletters?utm_source=TCUS&utm_medium=inline-link&utm_campaign=newsletter-text&utm_content=upper-coronavirus-facts">Sign up for The Conversation’s newsletter.</a>]</p><img src="https://counter.theconversation.com/content/139950/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Elizabeth McGraw 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>Epidemiological data suggests that 80% of COVID-19 cases can be traced to just 20% of those infected with SARS-CoV-2.Elizabeth McGraw, Professor of Entomology and Director of the Center for Infectious Disease Dynamics, Penn StateLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1365182020-04-17T01:51:24Z2020-04-17T01:51:24ZLatest coronavirus modelling suggests Australia on track, detecting most cases – but we must keep going<p>Late yesterday, epidemiologists from the Doherty Institute <a href="https://www.doherty.edu.au/uploads/content_doc/Estimating_changes_in_the_transmission_of_COVID-19_April14-public-release.pdf">released</a> what the Chief Medical Officer described as “<a href="https://www.health.gov.au/news/australian-health-protection-principal-committee-ahppc-coronavirus-covid-19-statement-on-16-april-2020">nowcasting</a>”: modelling that uses data from the previous 14 days to more accurately understand the present state of the COVID-19 epidemic.</p>
<p>In short, the findings are reassuring and suggest the inconvenience of social isolation is helping control the spread of SARS-CoV-2 in Australia. </p>
<p>It also indicates the spectre of “unidentified community transmission” is very unlikely indeed. This should be especially reassuring for healthcare workers, who may worry about coming into contact with COVID-positive patients presenting with a non-COVID problem.</p>
<p>What I don’t think it means, however, is that our outbreak control has been so effective that we should consider loosening the restrictions now. </p>
<h2>Overseas methods, Australian data</h2>
<p>The important thing to know is that this latest modelling uses Australian data.</p>
<p>One of the <a href="https://www.smh.com.au/politics/federal/a-matter-of-trust-experts-call-for-release-of-coronavirus-modelling-20200402-p54gfq.html">earlier criticisms</a> of the Australian government’s response to COVID-19 was that the expert advice was kept behind closed doors.</p>
<p>When the modelling was <a href="https://www.doherty.edu.au/news-events/news/covid-19-modelling-papers">made public</a>, those determined to find fault (especially on Twitter) pivoted to “But it’s based on overseas data!”</p>
<p>That’s not a criticism that can be levelled at this latest Doherty Institute modelling, which borrows methods developed by the London School of Tropical Medicine and Hygiene but uses really recent Australian data to build some estimates.</p>
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Read more:
<a href="https://theconversation.com/this-isnt-the-first-global-pandemic-and-it-wont-be-the-last-heres-what-weve-learned-from-4-others-throughout-history-136231">This isn't the first global pandemic, and it won't be the last. Here's what we've learned from 4 others throughout history</a>
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<h2>We are likely detecting most COVID-19 cases</h2>
<p>First, the modelling suggests there’s probably not some huge secret cohort of COVID-19 cases out there that we are not picking up due to insufficient testing. </p>
<p>The researchers compared the reported case-fatality rates (the proportion of COVID-19 positive people who died) in Australian states with that from a large <a href="https://www.medrxiv.org/content/10.1101/2020.03.09.20033357v1">Chinese study</a> (1.38%). </p>
<p>This is then used to infer the proportion of cases with symptoms which have been found by testing.</p>
<p>All states/territories have case detection rates above 80% – meaning that in each state, of all the people who have COVID-19 with symptoms, we are picking up about 80% or more. </p>
<p>If it wasn’t for the recent outbreaks in Tasmania, then all states would be above 90%. And in fact, the overall estimated case detection rate Australia-wide is 93%. Good news!</p>
<p>And as time goes on, the researchers are growing more certain about this conclusion (the technical term for this is the change in the “90% confidence interval” but in plain English that means the scientists are growing more confident these estimates are pretty accurate).</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=885&fit=crop&dpr=1 600w, https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=885&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=885&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1112&fit=crop&dpr=1 754w, https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1112&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/328566/original/file-20200416-192715-1c5hn9w.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1112&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 change in the light blue shaded area means scientists are growing more confident that their estimates are accurate as more Australian data becomes available.</span>
<span class="attribution"><span class="source">Doherty Institute</span></span>
</figcaption>
</figure>
<h2>An effective R below 1: meaning social distancing is working</h2>
<p>What scientists call the effective R is the way the virus spreads in a world where social distancing measures are in place. It refers to the average number of people each COVID-19 positive person is infecting. If it is below one, then it means the social distancing measures are working well.</p>
<p>The next model in the new Doherty Institute paper looks at the effective R ₀ in the six states over time. </p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=851&fit=crop&dpr=1 600w, https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=851&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=851&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=1070&fit=crop&dpr=1 754w, https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=1070&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/328567/original/file-20200416-192689-1c7qrxp.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=1070&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 effective R ₀ is under one in all states except Tasmania, but treat the Tasmanian data with caution: they have a small number of cases and a recent uptick, so that could be blowing out the average.</span>
<span class="attribution"><span class="source">Doherty Institute</span></span>
</figcaption>
</figure>
<p>In most states, the effective R has always been below one – indicating Australia has been effective at controlling spread since the beginning of the outbreak. </p>
<p>However, the numbers in Tasmania should be interpreted with caution. Their overall case numbers are small and they just had a big cluster, which affected their average disproportionately.</p>
<p>Crucially, the study team calculated the effective R based on cases identified as local transmission, rather than imported cases. That means, in real life, the effective R may be even better than this model estimates (because this estimate doesn’t account for border restrictions and quarantine of travellers).</p>
<p>In other words, this modelling is aiming to look at how effective our domestic control measures are. And the answer is: they’re working pretty well. </p>
<h2>Too soon to relax social distancing rules</h2>
<p>The social distancing measures take time to have an effect in stopping transmission. </p>
<p>It would also take time to become visible if we back off too early. </p>
<p>See-sawing our control measures would probably be far more disruptive than holding the course for just a little bit longer, and pose a risk of coronavirus rebound.</p><img src="https://counter.theconversation.com/content/136518/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Trent Yarwood does not work for, consult, own shares in or receive funding from any company or organisation that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.</span></em></p>The latest Doherty Institute modelling also indicates the spectre of ‘unidentified community transmission’ is very unlikely indeed.Trent Yarwood, Infectious Diseases Physician, Senior Lecturer, James Cook University and, The University of QueenslandLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1361432020-04-11T03:22:01Z2020-04-11T03:22:01ZHeadlines promise Australia’s on the ‘cusp’ of defeating coronavirus. We’re not and it’s too soon to relax restrictions<p>You might have seen <a href="https://www.news.com.au/world/coronavirus/australia/covid19-australia-on-cusp-of-coronavirus-dying-out/news-story/b0583e9f205a5f6df9e4219518a366e4">headlines</a> in the last day or so <a href="https://www.dailytelegraph.com.au/news/national/australia-on-the-cusp-of-defeating-the-coronavirus/video/d47ce246e0929951f619164e0559ff22">suggesting</a> Australia is on the “cusp” of defeating the coronavirus pandemic.</p>
<p>I’m here to say: make sure you read beyond the headlines. The reality (as acknowledged by many of the news reports, if you read them in full) is that while Australia is doing well, the social distancing measures will likely be in place for a good while yet.</p>
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Read more:
<a href="https://theconversation.com/coronavirus-what-causes-a-second-wave-of-disease-outbreak-and-could-we-see-this-in-australia-134125">Coronavirus: what causes a 'second wave' of disease outbreak, and could we see this in Australia?</a>
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<h2>On the cusp of what-now?</h2>
<p>The “cusp” headlines were based on <a href="https://www.health.gov.au/news/deputy-chief-medical-officers-press-conference-about-covid-19-on-10-april-2020">comments made on Friday by deputy chief medical officer Paul Kelly</a>, who told reporters “the average number of people that are infected by one person is a key component of understanding the virus and how it spreads”. He said:</p>
<blockquote>
<p>Ideally, where you want to be is below one, so less than one other person being infected after a person themselves had the infection. And once you get to that point the virus dies out or the epidemic dies out […]</p>
<p>And so at the moment we’re probably on the cusp of that in Australia. </p>
</blockquote>
<p>But an important part of his comment is what he said next:</p>
<blockquote>
<p>Now whether that’s where we are going to be in several weeks’ or months’ time remains to be seen.</p>
</blockquote>
<p>Paul Kelly is saying something quite specific here. He’s saying the early signs are encouraging and he is giving some positive feedback to people. </p>
<p>But his “cusp” comment is about a very specific aspect of infectious disease management: the R ₀ (pronounced R-nought).</p>
<h2>Basic R ₀ and effective R ₀: what’s the difference?</h2>
<p>The basic R ₀ tells us about how transmissible a disease is when everyone in the population is susceptible and there are no public health measures in place to control the disease. So this basic R ₀ is an inherent property of the infectious agent.</p>
<p>There’s also something called the effective R ₀, which is how the virus <em>really</em> spreads in the population. This effective R ₀ takes into account any immunity that people may have in the population as well as public health measures implemented to slow the spread of a disease.</p>
<p>When you get the effective R ₀ to less than one then you are on the way to seeing the virus disappear from the population. That’s because each person is spreading it to less than one person (on average).</p>
<p>That’s what Paul Kelly was explaining. Our social distancing measures are working and we are seeing the effective R ₀ under one, which means we are on the way to a really good outcome. </p>
<p>But it’s not quite true to say we are on the cusp of defeating the epidemic in Australia. </p>
<p>The only reason the effective R ₀ is less than one is <em>because</em> of those measures. As soon as you relax those restrictions, the effective R ₀ shoots up past one and you get exponential growth.</p>
<h2>The big question: community transmission</h2>
<p>At this stage of the epidemic, a large number of cases have been imported from overseas. So the great progress we are seeing now on the effective R ₀ may be because of the border controls and stopping transmission from cruise ships. </p>
<p>That’s good but you need to remember that to this point we have largely focused on testing those who have recently come from overseas or been in contact with someone recently returned.</p>
<p>It’s possible and likely that community transmission is occurring (where people are getting infected by someone who isn’t recently returned from overseas or a close contact of such a person).</p>
<p>Because our testing hasn’t focused on community transmission, we don’t know a lot about what’s happening in this space. However, we are now seeing testing criteria rapidly expand throughout the country so we will start to find out more about this in coming weeks.</p>
<h2>Good news but we need to keep going</h2>
<p>I do think Australia deserves some positive encouragement. We have done well, by and large, on the social distancing and we need to keep it up over Easter. Don’t undo all the hard work and all the gains we have made so far.</p>
<p>But whatever you do, don’t read these “cusp” headlines and walk away with the mistaken impression that we are on the cusp of the epidemic in Australia being over. That’s not where we are at right now. </p>
<p>As Paul Kelly said in the same press conference:</p>
<blockquote>
<p>on average, what we know about this virus if we don’t have these social distancing measures, one person can lead to 400 other cases within a month.</p>
</blockquote>
<p>Social distancing is one of our most important measures in stemming the epidemic. Australia needs to keep up the good work.</p>
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<strong>
Read more:
<a href="https://theconversation.com/grattan-on-friday-australias-coronavirus-debate-turns-to-the-way-out-136058">Grattan on Friday: Australia's coronavirus debate turns to the way out</a>
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<img src="https://counter.theconversation.com/content/136143/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Hassan Vally 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>I’m here to say: make sure you read beyond the headlines.Hassan Vally, Associate Professor, La Trobe UniversityLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1307772020-02-05T12:55:16Z2020-02-05T12:55:16ZR0: How scientists quantify the intensity of an outbreak like coronavirus and predict the pandemic’s spread<figure><img src="https://images.theconversation.com/files/313588/original/file-20200204-41516-vr3j0h.jpg?ixlib=rb-1.1.0&rect=622%2C142%2C7441%2C5341&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">To how many others will one infected person spread the infection?</span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/photo/large-group-of-people-royalty-free-image/937887974">Bim/E+ via Getty Images</a></span></figcaption></figure><p><em>Leer en <a href="https://theconversation.com/que-es-el-r0-el-numero-que-siguen-los-cientificos-para-ver-la-intensidad-del-coronavirus-137744">español</a></em></p>
<p>If you saw the 2011 movie “<a href="https://www.imdb.com/title/tt1598778/">Contagion</a>,” about a worldwide pandemic of a new virus, then you’ve heard the term “R0.” </p>
<p>Pronounced “R naught,” this isn’t just jargon made up in Hollywood. It represents an important concept in epidemiology and is a crucial part of public health planning during an outbreak, like the current coronavirus pandemic that’s spread globally since it was first identified in China.</p>
<p>Scientists use R0 – <a href="https://doi.org/10.3201/eid2501.171901">the reproduction number</a> – to describe the intensity of an infectious disease outbreak. R0 estimates have been an important part of characterizing pandemics or large publicized outbreaks, including the <a href="https://www.jstor.org/stable/20486145">2003 SARS pandemic</a>, the <a href="https://doi.org/10.1186/1471-2334-14-480">2009 H1N1 influenza pandemic</a> and the <a href="https://doi.org/10.1371/currents.outbreaks.91afb5e0f279e7f29e7056095255b288">2014 Ebola epidemic in West Africa</a>. It’s something epidemiologists are racing to nail down about SARS-CoV-2, the virus that causes COVID-19.</p>
<h2>How much will a disease spread?</h2>
<p>The formal definition of a disease’s R0 is the number of cases, on average, an infected person will cause during their infectious period. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=621&fit=crop&dpr=1 600w, https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=621&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=621&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=780&fit=crop&dpr=1 754w, https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=780&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/312353/original/file-20200128-120039-bogv2t.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=780&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">R0 describes how many cases of a disease an infected person will go on to cause – in this imagined scenario R0=2.</span>
<span class="attribution"><span class="source">The Conversation</span>, <a class="license" href="http://creativecommons.org/licenses/by-nd/4.0/">CC BY-ND</a></span>
</figcaption>
</figure>
<p>The term is used in two different ways. </p>
<p>The basic reproduction number represents the maximum epidemic potential of a pathogen. It describes what would happen if an infectious person were to enter a fully susceptible community, and therefore is an estimate based on an idealized scenario.</p>
<p>The effective reproduction number depends on the population’s current susceptibility. This measure of transmission potential is likely lower than the basic reproduction number, based on factors like whether some of the people are vaccinated against the disease, or whether some people have immunity due to prior exposure with the pathogen. Therefore, the effective R0 changes over time and is an estimate based on a more realistic situation within the population.</p>
<p>It’s important to realize that both the <a href="https://dx.doi.org/10.3201/eid2501.171901">basic and effective R0 are situation-dependent</a>. It’s affected by the properties of the pathogen, such as how infectious it is. It’s affected by the host population – for instance, how susceptible people are due to nutritional status or other illnesses that may compromise one’s immune system. And it’s affected by the environment, including things like demographics, socioeconomic and climatic factors.</p>
<p>For example, <a href="https://doi.org/10.1016/S1473-3099(17)30307-9">R0 for measles ranges from 12 to 18</a>, depending on factors like population density and life expectancy. This is a large R0, mainly because the measles virus is highly infectious.</p>
<p>On the other hand, the influenza virus is less infectious, with <a href="https://doi.org/10.1186/1471-2334-14-480">its R0 ranging</a> <a href="https://doi.org/10.1017/S0950268807009144">from 0.9 to 2.1</a>. Influenza, therefore, does not cause the same explosive outbreaks as measles, but it persists due to its ability to mutate and evade the human immune system. </p>
<h2>What makes R0 useful in public health?</h2>
<p>Demographer Alfred Lotka proposed the reproduction number in the 1920s, as a measure of the rate of reproduction in a given population.</p>
<p>In the 1950s, <a href="https://doi.org/10.1371/journal.ppat.1002588">epidemiologist George MacDonald suggested</a> using it to describe the transmission potential of malaria. He proposed that, if R0 is less than 1, the disease will die out in a population, because on average an infectious person will transmit to fewer than one other susceptible person. On the other hand, if R0 is greater than 1, the disease will spread.</p>
<p><iframe id="BOmTu" class="tc-infographic-datawrapper" src="https://datawrapper.dwcdn.net/BOmTu/7/" height="400px" width="100%" style="border: none" frameborder="0"></iframe></p>
<p>When public health agencies are figuring out how to deal with an outbreak, they are trying to bring R0 down to less than 1. This is tough for diseases like measles that have a high R0. It is <a href="https://www.cdc.gov/mmwr/PDF/rr/rr4711.pdf">especially challenging for measles in densely populated regions</a> like India and China, where R0 is higher, compared to places where people are more spread out.</p>
<p>For the <a href="https://doi.org/10.1126/science.1086478">SARS pandemic in 2003</a>, scientists estimated the original R0 to be around 2.75. A month or two later, the effective R0 dropped below 1, thanks to the tremendous effort that went into intervention strategies, including isolation and quarantine activities.</p>
<p>However, the pandemic continued. While on average, an infectious person transmitted to fewer than one susceptible individual, occasionally one person transmitted to tens or even hundreds of other cases. This phenomenon <a href="https://theconversation.com/what-is-a-super-spreader-an-infectious-disease-expert-explains-130756">is called super spreading</a>. Officials documented super spreader events a number of times during the SARS epidemic in Singapore, Hong Kong and Beijing.</p>
<figure class="align-center zoomable">
<a href="https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img alt="" src="https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=408&fit=crop&dpr=1 600w, https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=408&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=408&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=512&fit=crop&dpr=1 754w, https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=512&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/313590/original/file-20200204-41495-8uhzhq.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=512&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px"></a>
<figcaption>
<span class="caption">People in Hong Kong, concerned about coronavirus spreading from mainland China, wear face masks in February 2020.</span>
<span class="attribution"><a class="source" href="http://www.apimages.com/metadata/Index/Hong-Kong-China-Outbreak/3e0e13e1d7c44ce3a8439c982e27c797/1/0">AP Photo/Vincent Yu</a></span>
</figcaption>
</figure>
<h2>R0 for coronavirus SARS-CoV-2</h2>
<p>A number of groups have estimated R0 for this new coronavirus. The Imperial College group has estimated R0 to be <a href="https://www.imperial.ac.uk/mrc-global-infectious-disease-analysis/news--wuhan-coronavirus/">somewhere between 1.5 and 3.5</a>. Most modeling simulations that project future cases are using R0s in that range.</p>
<p>These differences are not surprising; there’s uncertainty about many of the factors that go into estimating R0, such as in estimating the number of cases, especially early on in an outbreak. </p>
<p>Based on these current estimates, projections of the future number of cases of coronavirus are fraught with high levels of uncertainty and will likely be somewhat inaccurate.</p>
<p>The difficulties arise for a number of reasons. </p>
<p>First, the basic properties of this viral pathogen – like the infectious period – are as yet unknown.</p>
<p>Second, researchers don’t know how many mild cases or infections that don’t result in symptoms have been missed by surveillance but nevertheless are spreading the disease.</p>
<p>Third, the majority of people who come down with this new coronavirus do recover, and are likely then immune to coming down with it again. It’s unclear how the changing susceptibility of the population will affect the future spread of infection. As the virus moves into new regions and communities, it encounters people with varying health conditions that affect their susceptibility to disease, as well as different social structures, both of which affect its transmissibility. </p>
<p>Finally, and likely the most important reason, no one knows the future impacts of current disease control measures. Epidemiologists’ current estimates of R0 say nothing about how measures such as <a href="https://www.washingtonpost.com/local/trafficandcommuting/white-house-considers-moving-all-of-europe-to-level-3-travel-advisory/2020/03/11/844090d0-63bc-11ea-b3fc-7841686c5c57_story.html">travel restrictions</a>, <a href="https://www.cdc.gov/coronavirus/2019-ncov/php/risk-assessment.html">social distancing</a> and <a href="https://theconversation.com/coronavirus-control-measures-arent-pointless-just-slowing-down-the-pandemic-could-save-millions-of-lives-133468">self-quarantine efforts</a> will influence the virus’s continued spread.</p>
<hr>
<p><em>This is an updated version of an article originally published on Feb. 5, 2020. The reproduction number for seasonal flu was corrected on March 27, 2020.</em></p><img src="https://counter.theconversation.com/content/130777/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Joseph Eisenberg 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>Epidemiologists want to quickly identify any emerging disease’s potential to spread far and wide. Dependent on a number of factors, this R0 number helps them figure that out and plan accordingly.Joseph Eisenberg, Professor and Chair of Epidemiology, University of MichiganLicensed as Creative Commons – attribution, no derivatives.