tag:theconversation.com,2011:/au/topics/b-1-1-7-97981/articlesB.1.1.7 – The Conversation2021-02-15T03:59:26Ztag:theconversation.com,2011:article/1552892021-02-15T03:59:26Z2021-02-15T03:59:26ZClose contact test results will be crucial to whether Auckland’s level 3 lockdown is extended beyond three days<figure><img src="https://images.theconversation.com/files/384178/original/file-20210215-13-co85q5.jpg?ixlib=rb-1.1.0&rect=40%2C100%2C4438%2C2713&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">
</span> <span class="attribution"><span class="source">Fiona Goodall/Getty Images</span></span></figcaption></figure><p>New Zealand’s latest community cases, the first to be infected with the more infectious B.1.1.7 variant of COVID-19, have a plausible link to the border through one person’s <a href="https://www.rnz.co.nz/news/national/436403/what-you-need-to-know-three-covid-19-community-cases-in-south-auckland">workplace at LSG Sky Chefs</a>, a business that deals with laundry and catering from international flights.</p>
<p>But it is not a definitive link. Indeed, Prime Minister Jacinda Ardern <a href="https://www.rnz.co.nz/news/national/436426/covid-19-auckland-cases-are-uk-variant-jacinda-ardern-says">announced this morning</a> that genome sequencing was not able to link the new infections to any cases we have seen recently in returned travellers. </p>
<p>Worryingly, this leaves the possibility of a more widespread community outbreak. </p>
<p>Even if a connection to the workplace can eventually be established, it may not be a direct human-to-human link. The LSG Sky Chefs worker is not thought to have had face-to-face contact with air crew or international travellers. </p>
<p>This means there may well be other cases in the chain of transmission between the border and the worker, and these cases could have sparked additional community transmission chains. </p>
<p>This makes the situation potentially more dangerous than the recent cases associated with the <a href="https://www.rnz.co.nz/news/national/435296/two-more-people-linked-with-pullman-hotel-treated-as-confirmed-covid-cases">Pullman hotel managed isolation facility</a>, which had a clear and direct link to the border. </p>
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Read more:
<a href="https://theconversation.com/its-still-too-soon-for-nz-to-relax-covid-19-border-restrictions-for-travellers-from-low-risk-countries-154643">It's still too soon for NZ to relax COVID-19 border restrictions for travellers from low-risk countries</a>
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<h2>More contagious variant</h2>
<p>Auckland returned to level 3 lockdown conditions at midnight on Sunday following the announcement of the three new cases. The rest of the country moved to alert level 2, with both restrictions in place until at least Wednesday this week. </p>
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<img alt="A window display at Auckland's Papatoetoe High School, showing paper cut-out figures." src="https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/384181/original/file-20210215-19-1vlggi7.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">A window display at Auckland’s Papatoetoe High School, where one of the new cases is a student.</span>
<span class="attribution"><span class="source">Fiona Goodall/Getty</span></span>
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</figure>
<p>Genome sequencing has revealed the new community cases <a href="https://www.health.govt.nz/news-media/media-releases/update-genomic-sequencing">have the more infectious B.1.1.7 lineage</a>. This variant (also known as VOC-202012/01) was first identified in the UK late last year. Since then it has rapidly become dominant across England. </p>
<p>It has also sparked outbreaks that have led to short, sharp restrictions in the Australian states of <a href="https://www.rnz.co.nz/news/world/434210/brisbane-locks-down-to-halt-spread-of-covid-variant">Queensland</a>, <a href="https://www.abc.net.au/news/2021-02-06/wa-covid-lockdown-successful-but-luck-a-factor-experts-say/13127384">Western Australia</a>, and most recently <a href="https://www.theguardian.com/australia-news/2021/feb/13/epidemiologists-back-victorias-lockdown-but-say-evidence-not-yet-in-on-shorter-incubation">Victoria</a>.</p>
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Read more:
<a href="https://theconversation.com/yes-another-lockdown-in-victoria-hurts-but-it-might-be-our-only-way-to-avert-a-third-wave-155212">Yes, another lockdown in Victoria hurts. But it might be our only way to avert a third wave</a>
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<p>The UK has one of the best COVID-19 <a href="https://www.cogconsortium.uk/">genomic surveillance systems</a> and this has allowed scientists to track the spread of B.1.1.7. <a href="https://www.medrxiv.org/content/10.1101/2020.12.30.20249034v2">Multiple lines of evidence</a> now point to an increase in the reproductive number of the virus. </p>
<p>This number, often called R0, is the average number of people each infected person will go on to infect. Researchers in the UK recently <a href="https://cmmid.github.io/topics/covid19/uk-novel-variant.html">estimated R0 to be 43-82% higher</a> for B.1.1.7 than for previous variants. </p>
<p>This is why moving Auckland to alert level 3 was the right thing to do. Given the highly infectious nature of the B.1.1.7 variant, and the chance these infections may have come from a source other than the family member’s workplace, there may be another cluster of cases out there that we don’t know about yet. </p>
<p>We know that some family members travelled to New Plymouth, in the Taranaki region, during the Waitangi weekend. There is a risk they passed the virus on to others, but there is also a reasonable chance this was before their infectious period. </p>
<p>At this point, it would seem unnecessary to place the Taranaki region under stricter lockdown conditions. We will know more later in the week, once results are in from tests of people who visited locations of interest in Taranaki. </p>
<h2>Short lockdown or bigger outbreak</h2>
<p>There are two main questions that need to be answered before we can consider relaxing alert levels for Auckland and the rest of the country. Firstly, we need to find out whether any of the three known cases passed the virus on to others in the community. </p>
<p>Anyone who lives in Auckland or Taranaki, or has travelled through Auckland or Taranaki in the last week should check the <a href="https://www.health.govt.nz/our-work/diseases-and-conditions/covid-19-novel-coronavirus/covid-19-health-advice-public/contact-tracing-covid-19/covid-19-contact-tracing-locations-interest#auckfeb">Ministry of Health website</a> to see if they were at any of the locations of interest at the times listed. </p>
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<p>If so, exposure to the virus is possible and anyone should follow the instructions on the website. If all those who may have been exposed can be identified quickly, the government will feel more confident about relaxing alert levels in the next few days.</p>
<p>But secondly, we also need to know if there are other chains of transmission stemming from cases in between the border and the family. Testing of close and “casual plus” contacts of the three cases will help answer this over the coming days. Testing of people connected with the LSG Sky Chefs workplace and Papatoetoe High School will be particularly important. </p>
<p>Finally, if there are cases that were infected prior to the three cases announced on Sunday, the virus could have been spreading in the community undetected for several weeks. Modelling shows that if there are additional cases upstream of the LSG Sky Chefs worker, the outbreak may already have infected more than 50 people. </p>
<p>But if we can rule this out by establishing a direct link to the source of infection, the outbreak is likely to be much smaller. </p>
<p>If we find significant community transmission, we need to be prepared for alert level 3 restrictions to last several weeks. Because we are dealing with a more transmissible variant, it is even possible <a href="https://theconversation.com/why-the-covid-19-variants-are-so-dangerous-and-how-to-stop-them-spreading-153535">we might need to move to alert level 4</a> to contain and eliminate the outbreak.</p><img src="https://counter.theconversation.com/content/155289/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Michael Plank is affiliated with the University of Canterbury and receives funding from the Ministry of Business, Innovation and Employment (MBIE) and Te Pūnaha Matatini, New Zealand's Centre of Research Excellence in complex systems. </span></em></p><p class="fine-print"><em><span>Shaun Hendy is affiliated with the University of Auckland and receives funding from the Ministry of Business, Innovation and Employment (MBIE) and Te Pūnaha Matatini, New Zealand's Centre of Research Excellence in complex systems.</span></em></p><p class="fine-print"><em><span>Siouxsie Wiles is affiliated with the University of Auckland and receives funding from the Ministry of Business, Innovation and Employment (MBIE) and Te Pūnaha Matatini, New Zealand's Centre of Research Excellence in complex systems.</span></em></p>The highly infectious nature of the COVID-19 variant, and the fact the infections have no clear link to the border, leaves the worrying possibility of a more widespread community outbreak.Michael Plank, Professor in Applied Mathematics, University of CanterburyShaun Hendy, Professor of Physics, University of Auckland, Waipapa Taumata RauSiouxsie Wiles, Associate Professor in Microbiology and Infectious Diseases, University of Auckland, Waipapa Taumata RauLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1535302021-01-21T21:48:37Z2021-01-21T21:48:37ZWhy new COVID-19 variants are on the rise and spreading around the world<figure><img src="https://images.theconversation.com/files/380025/original/file-20210121-17-1r712y0.jpg?ixlib=rb-1.1.0&rect=137%2C101%2C3730%2C2544&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">Medical technician Amira Doudou prepares samples at the University Hospital Institute for Infectious Diseases in Marseille, France, Jan. 13, 2021, to study the highly contagious COVID-19 variant.</span> <span class="attribution"><span class="source">(AP Photo/Daniel Cole)</span></span></figcaption></figure><p>A new variant of coronavirus has swept across the United Kingdom and been detected in the United States, Canada and elsewhere. <a href="https://www.who.int/news/item/12-01-2021-global-scientists-double-down-on-sars-cov-2-variants-research-at-who-hosted-forum">Scientists are concerned</a> that these new strains may spread more easily. </p>
<p>As an evolutionary biologist, I study how mutation and selection combine to shape changes in populations over time. Never before have we had so much real-time data about evolution as we do with SARS-CoV-2: over <a href="https://www.gisaid.org">380,000 genomes</a> were sequenced last year.</p>
<p>SARS-CoV-2 has been mutating as it spreads, generating slight differences in its genome. These mutations allow scientists to trace who is related to whom across the <a href="https://nextstrain.org/ncov/global">family tree</a> of the virus.</p>
<p>Evolutionary biologists, including myself, have cautioned against over-interpreting the threat posed by mutations. Most mutations will not help the virus, just like randomly kicking a working machine is unlikely to make it better. </p>
<p>But every once in a while a mutation or suite of mutations gives the virus an advantage. The data are convincing that the mutations carried by the variant that first appeared in the U.K., known as B.1.1.7, make the virus more “fit.”</p>
<h2>Higher fitness or chance?</h2>
<p>When a new variant becomes common, scientists determine the reason behind its spread. A virus carrying a particular mutation can rise in frequency by chance if it is:</p>
<ul>
<li>carried by a superspreader;</li>
<li>moved to a new uninfected location;</li>
<li>introduced into a new segment of the population.</li>
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<p>The latter two examples are called “founder events”: a rapid rise in frequency can occur if a particular variant is introduced into a new group and starts a local epidemic. Chance events may explain the <a href="https://doi.org/10.1016/j.cub.2020.06.031">rise in frequency of several different SARS-CoV-2 variants</a>. </p>
<p>But B.1.1.7 is an exception. It shows a very strong signal of selection. For the past two months, B.1.1.7 has risen in frequency faster than non-B.1.1.7 in virtually every week and health region in England. <a href="https://www.gov.uk/government/publications/investigation-of-novel-sars-cov-2-variant-variant-of-concern-20201201">This data, reported</a> on Dec. 21, 2020, helped convince U.K. <a href="https://www.cnn.com/videos/world/2021/01/04/boris-johnson-full-speech-coronavirus-variant-england-lockdown-vpx.cnn">Prime Minister Boris Johnson to place much of the country under lockdown</a> and led to widespread travel bans from the U.K. </p>
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<p>The rise of B.1.1.7 cannot be explained by a founder event in new regions, because COVID-19 was already circulating across the U.K. Founder events in a new segment of the population (e.g., following a conference) also aren’t plausible given the widespread restrictions against large gatherings at the time.</p>
<p>Our ability to track the evolution of SARS-CoV-2 is due to the massive effort by scientists to share and analyze data in real time. But the incredibly detailed knowledge we have about B.1.1.7 is also due to just plain dumb luck. One of its mutations altered a section of the genome used to test for COVID-19 in the U.K., allowing <a href="https://virological.org/t/transmission-of-sars-cov-2-lineage-b-1-1-7-in-england-insights-from-linking-epidemiological-and-genetic-data/576">the picture of evolutionary spread to be drawn from more than 275,000 cases</a>. </p>
<h2>Evolution in action</h2>
<p>Epidemiologists have concluded that B.1.1.7 is more transmissible, but there are no signs that it is more deadly. Some researchers estimate that B.1.1.7 increases the number of new cases caused by an infected individual (called the reproductive number or Rt) by between <a href="https://virological.org/t/transmission-of-sars-cov-2-lineage-b-1-1-7-in-england-insights-from-linking-epidemiological-and-genetic-data/576">40 and 80 per cent</a>; another preliminary study found that <a href="https://doi.org/10.1101/2020.12.24.20248822">Rt increased by 50-74 per cent</a>.</p>
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<img alt="A women pushing a cart through a nearly empty airport." src="https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=420&fit=crop&dpr=1 600w, https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=420&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=420&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=528&fit=crop&dpr=1 754w, https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=528&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/380037/original/file-20210121-15-1xmrigt.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=528&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">A woman pushes a luggage cart through Heathrow Airport in London, on Jan. 18, 2021.</span>
<span class="attribution"><span class="source">(AP Photo/Matt Dunham)</span></span>
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</figure>
<p>A 40-80 per cent advantage means that B.1.1.7 isn’t just a little more fit, it’s a lot more fit. Even when selection is this strong, evolution isn’t instantaneous. Our mathematical modelling, as well as that by <a href="https://covid19-sciencetable.ca/wp-content/uploads/2021/01/Update-on-COVID-19-Projections_January-12-2021_Final_English-2.pdf">others in Canada</a> and the <a href="https://www.nytimes.com/live/2021/01/16/world/covid-19-coronavirus#a-fast-spreading-variant-could-become-the-dominant-source-of-infection-in-the-us-by-march-cdc-says">U.S.</a>, shows that it takes B.1.1.7 a couple of months to reach its meteoric rise, because only a small fraction of cases initially carries the new variant. </p>
<p>For many countries, like the U.S. and Canada, where the number of COVID-19 cases has been precariously rising, a variant that increases transmission by 40-80 per cent threatens to push us over the top. It could lead to exponential growth in cases and overwhelm already threadbare medical care. Evolutionary change takes a while, buying us maybe a few weeks to prepare. </p>
<h2>More variants</h2>
<p>One surprise for researchers was that B.1.1.7 bears a remarkable number of new mutations. B.1.1.7 has accumulated 30-35 changes over the past year. B.1.1.7 doesn’t mutate at a higher rate, but it appears to have undergone a bout of rapid change in the recent past. </p>
<figure class="align-center ">
<img alt="" src="https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" srcset="https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=489&fit=crop&dpr=1 600w, https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=489&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=489&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=614&fit=crop&dpr=1 754w, https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=614&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/379429/original/file-20210119-23-1p1uyv7.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=614&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">Each dot represents a SARS-CoV-2 genome, with branches connecting related viruses to their ancestors. The centre representss the virus introduced into humans. The viruses furthest from the centre carry more mutations. Highlighted in gold are the three new variants.</span>
<span class="attribution"><a class="source" href="https://www.nextstrain.org">(NextStrain)</a>, <a class="license" href="http://creativecommons.org/licenses/by/4.0/">CC BY</a></span>
</figcaption>
</figure>
<p>The virus may have been <a href="https://www.gov.uk/government/publications/investigation-of-novel-sars-cov-2-variant-variant-of-concern-20201201">carried by an immunocompromised individual</a>. People with weaker immune systems fight the virus constantly, with prolonged infections, recurrent rounds of viral replication and only a partial immune response to which <a href="https://doi.org/10.1056/NEJMc2031364">the virus is constantly evolving</a>.</p>
<p>Preliminary research reports that have yet to be verified have described two other variants of concern: one originally from <a href="https://www.doi.org/10.1101/2020.12.21.20248640">South Africa (B.1.351)</a> and one from <a href="https://virological.org/t/genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-manaus-preliminary-findings/586">Brazil (P1)</a>. Both variants show a recent history of excess mutations and rapid increases in frequency within local populations. Scientists are currently gathering the data needed to confirm that selection for higher transmission, not chance, is responsible.</p>
<h2>What changed to allow spread?</h2>
<p>Selection plays two roles in the evolution of these variants. First consider the role within those individuals in which the large number of mutants arose. <a href="https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563">B.1.1.7’s 23 mutations</a> and P1’s 21 mutations aren’t randomly arrayed across the genome but clustered in the gene encoding the <a href="https://theconversation.com/new-coronavirus-variant-what-is-the-spike-protein-and-why-are-mutations-on-it-important-152463">spike protein</a>.</p>
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<strong>
Read more:
<a href="https://theconversation.com/new-coronavirus-variant-what-is-the-spike-protein-and-why-are-mutations-on-it-important-152463">New coronavirus variant: what is the spike protein and why are mutations on it important?</a>
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<p>One change in the spike, called N501Y, arose independently in all three variants, as well as in immunocompromised patients studied in the <a href="https://doi.org/10.1056/NEJMc2031364">U.S.</a> and <a href="https://doi.org/10.1101/2020.12.05.20241927">U.K.</a> Other changes in the spike (e.g. E484K, del69-70) are seen in two of the three variants.</p>
<p>Beyond the spike, the three variants of concern share one additional mutation that deletes a small part of the drably named “non-structural protein 6” (NSP6). We don’t yet know what the deletion does, but <a href="https://doi.org/10.4161/auto.29309">in a related coronavirus NSP6 tricks a cellular defence system and may promote coronavirus infection</a>. NSP6 also hijacks this system to help <a href="https://doi.org/10.1080/15548627.2020.1817280">copy the viral genome</a>. Either way, the deletion might alter the ability of the virus to take hold and replicate within our cells.</p>
<h2>Easier transmission</h2>
<p>The parallel evolution of the same mutations in different countries and in different immunocompromised patients suggests that they convey a selective advantage to evade the immune systems of the individuals in which the mutations occurred. For N501Y, this has been backed up by experiments <a href="https://doi.org/10.1126/science.abc4730">in mice</a>. </p>
<p>But what accounts for the higher transmission rate from individual to individual? This is challenging to answer because the many mutations that arose at once are now bundled together in these variants, and it could be any one or a combination of them that leads to the transmission advantage.</p>
<p>That said, several of these variants have arisen before on their own and haven’t led to rapid spread. One study showed that <a href="https://doi.org/10.1101/2020.12.20.20248581">N501Y had only a weak transmission advantage on its own</a>, rising rapidly only when coupled with the suite of mutations observed in B.1.1.7. </p>
<p>While the evolutionary story of COVID is still being written, one important message is emerging now. The 40-80 per cent transmission advantage of B.1.1.7, and potentially the other variants B.1.351 and P1, <a href="https://www.nytimes.com/live/2021/01/16/world/covid-19-coronavirus#a-fast-spreading-variant-could-become-the-dominant-source-of-infection-in-the-us-by-march-cdc-says">will overwhelm many countries in the next few months</a>. </p>
<p>We’re in a race against viral evolution. We must roll out vaccines as quickly as possible, stem the flow of variants by restricting interactions and travel, and get in front of spread by ramping up surveillance and contact tracing.</p><img src="https://counter.theconversation.com/content/153530/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>Sarah Otto volunteers on the BC COVID-19 Modelling Group, the Board of The Nature Trust of British Columbia, and on the Species at Risk Advisory Committee to Canada's Minister of the Environment. She receives research funding from the Natural Sciences and Engineering Research Council of Canada.</span></em></p>Multiple COVID-19 variants are circulating around the world and becoming more common. These mutations can alter the ability of the virus to take hold and replicate within our cells.Sarah Otto, Killam University Professor in Evolutionary Biology, University of British ColumbiaLicensed as Creative Commons – attribution, no derivatives.tag:theconversation.com,2011:article/1523832020-12-22T13:37:07Z2020-12-22T13:37:07ZWhy it matters that the coronavirus is changing – and what this means for vaccine effectiveness<figure><img src="https://images.theconversation.com/files/376208/original/file-20201221-15-14a61bi.jpg?ixlib=rb-1.1.0&rect=11%2C29%2C3958%2C2473&q=45&auto=format&w=496&fit=clip" /><figcaption><span class="caption">The French government will not accept any passengers arriving from the U.K. amid fears over the new mutant coronavirus strain. </span> <span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/news-photo/police-and-port-staff-at-the-port-of-dover-in-kent-which-news-photo/1230247432?adppopup=true">Steve Parsons/PA Images via Getty Images</a></span></figcaption></figure><p><a href="https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563">A new variant of SARS-CoV-2</a> is spreading rapidly in the United Kingdom, with over <a href="https://www.cogconsortium.uk/wp-content/uploads/2020/12/Report-1_COG-UK_19-December-2020_SARS-CoV-2-Mutations.pdf">1,400 cases</a> since September. SARS-CoV-2, the virus that causes COVID-19, generally <a href="https://doi.org/10.1093/ve/veaa061">accumulates mutations slowly over time</a>, but this new variant had <a href="https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563">accumulated many mutations quickly</a>.</p>
<p>If this new version of the virus is here to stay, as it appears to be, what does that mean? Will this new version of the virus replace the old one? Will it be easier to catch? And, most important, will the current vaccines still be effective? </p>
<p>This interests me because I am an <a href="https://scholar.google.com/citations?user=VkV9_zoAAAAJ&hl=en">evolutionary microbiologist</a> who studies the link between the <a href="https://doi.org/10.1371/journal.pbio.2004444">transmission and evolution of infectious diseases</a>. In particular, I spend a lot of time considering the effects of <a href="https://doi.org/10.1371/journal.pbio.1002198">vaccines on pathogen evolution</a> and the effects of <a href="https://doi.org/10.1073/pnas.1717159115">pathogen evolution on the impact of vaccines</a>. </p>
<h2>What is the new SARS-CoV-2 mutant that has emerged?</h2>
<figure class="align-right ">
<img alt="" src="https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=237&fit=clip" srcset="https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=600&fit=crop&dpr=1 600w, https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=600&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=600&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=754&fit=crop&dpr=1 754w, https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=754&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/376214/original/file-20201221-23-1bdb687.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=754&fit=crop&dpr=3 2262w" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px">
<figcaption>
<span class="caption">As the spike proteins on the surface the SARS-CoV-2 virus mutate the shape changes, which may affect the ability of the coronavirus to infect cells.</span>
<span class="attribution"><a class="source" href="https://www.gettyimages.com/detail/illustration/vector-illustration-of-viruses-royalty-free-illustration/1219220412?adppopup=true">Tharun15/iStock via Getty Images Plus</a></span>
</figcaption>
</figure>
<p>The new version of SARS-CoV-2 – named the B.1.1.7 lineage – is spreading in the U.K. and possibly beyond. The differences between the old and new virus include <a href="https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563">23 mutations in the virus’s genetic code that have altered four viral proteins</a>. </p>
<p><a href="https://www.cogconsortium.uk/wp-content/uploads/2020/12/Report-1_COG-UK_19-December-2020_SARS-CoV-2-Mutations.pdf">Eight of these 23 mutations affect the spike protein</a>. This matters because the spike protein enables the virus to enter human cells, and it is a key target of our immune response, both in fighting off <a href="https://doi.org/10.1016/j.cell.2020.09.037">the virus during infection</a> and in <a href="http://doi.org/10.1056/NEJMoa2034577">protecting us from disease following vaccination</a> with the Pfizer and Moderna vaccines. </p>
<p>If the changes to the spike protein help the virus enter human cells more easily, then the virus could be transmitted from person to person more readily.</p>
<p>These mutations may also alter how well the host’s immune system combats the virus, potentially reducing the efficacy of the current vaccines. </p>
<h2>What is different about this new version of SARS-CoV-2?</h2>
<p>Samples of the new virus isolated from patients suggest that this variant has been <a href="https://www.cogconsortium.uk/wp-content/uploads/2020/12/Report-1_COG-UK_19-December-2020_SARS-CoV-2-Mutations.pdf">increasing in relative frequency</a> over the past three months. </p>
<p>The increase in frequency is concerning, as it suggests – <a href="https://www.sciencemag.org/news/2020/12/mutant-coronavirus-united-kingdom-sets-alarms-its-importance-remains-unclear">but does not prove</a> – that the B.1.1.7 isolates of SARS-CoV-2 are more transmissible than the original virus. Some have estimated that the new virus may be up to <a href="https://www.wsj.com/articles/what-we-know-about-the-new-covid-19-strain-in-england-11608423416">70% more transmissible than the old virus</a>. While these estimates are <a href="https://khub.net/documents/135939561/338928724/SARS-CoV-2+variant+under+investigation%2C+meeting+minutes.pdf/962e866b-161f-2fd5-1030-32b6ab467896?t=1608470511452">consistent with the data</a>, it is entirely too early to make a definitive conclusion.</p>
<p>If this increase in transmissibility is confirmed, it might be due to of the <a href="https://doi.org/10.1126/science.abc4730">mutations in the spike protein</a> allows it to bind more tightly to the <a href="https://theconversation.com/what-is-the-ace2-receptor-how-is-it-connected-to-coronavirus-and-why-might-it-be-key-to-treating-covid-19-the-experts-explain-136928">ACE2 receptor</a>, which provides a gateway for the virus to enter human cells. </p>
<p>But it might also be due to any of the other changes to the virus. </p>
<h2>Is it more dangerous? If so, why?</h2>
<p>If the new version, B.1.1.7, is indeed more transmissible than the old virus, it will be more dangerous in the sense that it will make more people sick. </p>
<p>However, I am not aware of <a href="https://khub.net/documents/135939561/338928724/SARS-CoV-2+variant+under+investigation%2C+meeting+minutes.pdf/962e866b-161f-2fd5-1030-32b6ab467896?t=1608470511452">good evidence that there is any difference in severity</a> of disease caused by the new version of this virus compared with the older one. That said, with so <a href="https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563">few known cases</a>, it may still be too early to say. </p>
<h2>Will the Pfizer and Moderna vaccines still be effective against this new strain?</h2>
<p>Both the <a href="https://theconversation.com/how-mrna-vaccines-from-pfizer-and-moderna-work-why-theyre-a-breakthrough-and-why-they-need-to-be-kept-so-cold-150238">Pfizer and Moderna vaccines work by training our immune systems</a> to recognize a <a href="https://doi.org/10.1056/NEJMoa2027906">specific version of the viral spike protein</a>. The version of the spike protein used by the vaccines was designed to match that of the old virus, not that of the B.1.1.7 virus. This means that the vaccines might become less effective than expected should this new virus spread widely. </p>
<p>Vaccine-virus mismatch is an ongoing challenge for scientists charged with developing the seasonal flu vaccine. But <a href="https://doi.org/10.1186/1741-7015-11-153">even with a virus-vaccine mismatch</a>, the flu vaccine reduces the likelihood, and the severity, of disease. </p>
<p>The question is therefore not whether the vaccines will be effective, but rather how effective they will be. The severity of the mismatch matters, but the only way to determine <a href="https://doi.org/10.1371/journal.pbio.3001000">its impact in this case is through scientific study</a>, and to my knowledge, no data on that has yet been collected. In other words, it’s too early to say whether and how this new variant will influence the overall effectiveness of the Pfizer and Moderna vaccines.</p>
<h2>Should people still get the new mRNA vaccine?</h2>
<p>The appearance of this new B.1.1.7 makes it even more important that people get vaccinated as soon as possible. </p>
<p>If this new version is more transmissible, or if the vaccine is less effective because of a virus-vaccine mismatch, <a href="https://arxiv.org/abs/2006.14676">more people will need to be vaccinated</a> to achieve herd immunity and get this disease under control. </p>
<p>Moreover, we now have proof that the spike protein of SARS-CoV-2 can change drastically in a short time, and so it is critical that we <a href="https://doi.org/10.1098/rspb.2016.2562">get the virus under control to prevent it from evolving</a> further and completely undermining vaccination efforts.</p><img src="https://counter.theconversation.com/content/152383/count.gif" alt="The Conversation" width="1" height="1" />
<p class="fine-print"><em><span>David Kennedy 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>A new strain of the SARS-CoV-2 virus that causes COVID-19 appears to be spreading fast in the UK. This probably isn’t a big problem, but the data isn’t in yet.David Kennedy, Assistant Professor of Biology, Penn StateLicensed as Creative Commons – attribution, no derivatives.