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COVID-19 THE EVOLVING VIRUS Everything you What it means How long before need to know about for the roll-out this is just the new variants of another cold?

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Time to adapt As the coronavirus mutates, we will need to adjust our approach to it

JUST one month ago, the world Now the virus has picked up need for tweaks to vaccines or new was already struggling to contain mutations that allow it to spread treatments (see page 10). the spread of the coronavirus. more easily and, in some cases, The news of these new variants has Now the challenge has become that could help it evade our coincided closely with the widespread even harder. The emergence of new immune system (see page 8). and very welcome roll-out of vaccines variants with different properties has A faster-spreading virus leads against covid-19. These vaccines offer changed the rules of engagement. to more , as has been seen us a way out of the pandemic, but we That the coronavirus should evolve already knew it would be a long road isn’t surprising – this is what viruses “A virus that can evade our to vaccinating almost the entire adult do. Scientists have been sequencing the immune system has the population of the globe. The recent genome of the SARS-CoV-2 virus since it potential to reinfect people” evolution of the virus shows us just how began spreading out of Wuhan in China, long and complicated that road could be. recording the mutations that naturally in the UK and several other countries, As we try to work out how best accumulate as more and more people and thus, inevitably, to more deaths. to counter these variants, and what become infected and pass it on. An “escape mutant” virus that tweaks may need to be made to our This virus evolves mercifully slowly. can evade our immune response, vaccines, there is really only one Until recently, the genetic changes meanwhile, has the potential to reinfect thing we know for certain: the only we saw were of little consequence those who have already had covid-19. way to stop the virus from evolving to us, but that has begun to change. Such a variant might even lead to the is to stop it from spreading. ❚

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23 January 2021 | New Scientist | 5 News Coronavirus

Mutant variants The coronavirus evolves Several new viral variants pose added threats – how worried should we be?

Graham Lawton

THE rise and spread of new now circulating worldwide “We are now rolling out terrifying”, says Robertson. pressure. In May 2020, an Days later, Gupta’s team saw a variants of the coronavirus are carry this mutation. vaccination to high-risk groups “It is a concern that a large immunocompromised patient dramatic rise in a mutant version seen as ushering in a dangerous More recently, three other and this is going to provide a very number of spike mutations was admitted to a UK hospital with of the coronavirus and later new phase of the covid-19 mutants, known as the UK, South strong selection pressure,” says are found in the same strain,” covid-19. He died of the disease in confirmed that it had partially pandemic. But from the virus’s African and Brazilian variants, Emma Thomson at the University says Kumar. August. Over the 101-day course of escaped the therapeutic effects perspective, nothing has changed. have also started spreading of Glasgow. “We may well see a One potential danger that we his illness, a team led by Ravindra of the plasma. This mutant virus It is just doing what comes rapidly. All are also thought to rapid rise in mutations as a result.” can probably stop worrying about Gupta at the University of eventually killed the patient. naturally to viruses: evolving. have mutations that make them We will also have to keep an is recombination, which occurs Cambridge repeatedly sampled We mustn’t draw too many It is now well-established that more transmissible, and some eye out for viruses that can evade when two related coronaviruses and sequenced viruses from the conclusions from this single case, SARS-CoV-2 is a coronavirus with might be able to outsmart parts natural immunity, she says. mash their genomes together patient’s respiratory tract. says Gupta. The patient was also a large and unusually stable RNA Virologists have already to create a hybrid. Two studies being treated for cancer and “We are rolling out vaccines genome, but that doesn’t mean discovered variants that are able scouring thousands of viral The virus strikes back couldn’t mount an effective it doesn’t change at all. Unlike to high-risk groups. We to partially evade antibodies. genomes have found no evidence immune response of his own. But most other RNA viruses, which are may well see a rapid rise These are a wake-up call. Even that this has occurred. The patient was given infusions the study shows how quickly and among the most mutation-prone in mutations as a result” though the UK variant, known as But escape mutation is a real of an antiviral therapy called viciously the virus can mutate and biological entities in the world, B.1.1.7, doesn’t seem to have an and present danger. A recent convalescent plasma – an escape under selection pressure. SARS-CoV-2’s genome changes of the immune system, although escape mutation, the fact that its case study highlights what antibody-rich blood extract The answer to these threats is very slowly. This is largely because they don’t seem to be more deadly. spike protein is 17 mutations away could happen once we put from another person infected surveillance, to flag up and isolate it has a proofreading function The sudden appearance of from the original is “a little bit the virus under heavy selection with the virus. escape mutants before they spiral that is efficient at eliminating these three new variants doesn’t out of control. The UK’s world- errors during replication, a major suggest that the virus has upped class surveillance system relies on source of the genetic variation its mutation rate, says Sudhir What are the new coronavirus variants? a combination of monitoring and that we call evolution. Kumar at Temple University sequencing. Red flags are raised “There’s not masses of in Pennsylvania. They are an THERE are tens of thousands Denmark and Switzerland. It has to both viruses, known as N501Y. if something unusual happens evolution occurring, this is inevitable product of time and lots of variants of the SARS-CoV-2 reached many other countries, However, this was first seen last clinically or epidemiologically, and a very slow-evolving virus,” LIBRARY PHOTO GAERTNER/SCIENCE JUAN of transmission events between virus that differ from each too, but because most countries April, in Brazil, and a variant with then geneticists search for mutant says David Robertson at the people. Under such circumstances, other by at least one mutation, sequence far fewer samples it circulated in Wales for a while, viruses that could be responsible. MRC-University of Glasgow Centre Illustration of the One arm of our innate immune new variants are bound to arise according to sequencing studies than the UK or Denmark do, so this alone cannot explain the The new UK variant, for for Virus Research in the UK. B.1.1.7 coronavirus system is a generalised antiviral by chance. Highly transmissible that track its spread and monitor it isn’t yet clear whether it is higher transmissibility. example, was spotted because A project called Nextstrain, variant’s spike weapon that introduces random ones have a biological advantage how it is evolving. outcompeting other variants With many countries now lockdown restrictions were based at the Fred Hutchinson protein (red) errors into viral genomes in a bid and so will outcompete their Many of these variants die in these countries as well. looking for the new variants, reducing viral spread everywhere Cancer Research Center in Seattle, to neutralise them. It doesn’t more sluggish rivals. out, but others spread and Initial studies suggest that reports are emerging of other but Kent. Surveillance would also compiles all published viral always succeed. More variants are inevitable. “As acquire further mutations. B.1.1.7 is about 50 per cent versions with similar changes. genome sequences and plots Most of the surviving mutations the virus mutates, this story will Overall, though, the coronavirus more transmissible than other In particular, the P.1 variant found “Even though this virus them on a family tree. This are of no medical significance. keep repeating itself,” says Sharon hasn’t changed much. Any two variants. This might not sound in Brazil has nearly the same is evolving slowly, we shows the original virus, called Up until now, the virus has been Peacock, head of the COVID-19 SARS-CoV-2 coronaviruses like much, but it makes a huge three mutations in the spike have to take surveillance Wuhan-Hu-1, diverging steadily circulating unhindered in a Genomics UK Consortium. The from anywhere in the world difference over time. protein as B.1.351. very, very seriously” as it spread around the world. large host population with big worry is the emergence of will usually differ by fewer than Another new variant, known as Reports of two new variants The virus’s average mutation little immunity, and hence “escape mutations” that enable 30 mutations, and they are all B.1.351, was discovered in South have also emerged in the US, be triggered if vaccinated people rate remains low and steady has encountered minimal the virus to dodge the immune still regarded as one strain. Africa after an unusual surge in one of which also has the or those who had recovered at about two mutations per resistance, or selection pressure system or render vaccines or In early December, scientists coronavirus cases beginning N501Y mutation, as well as started falling ill, says Kumar. lineage per month, but over time as evolutionary biologists call it. drugs useless (see page 10). looking for reasons for a rapid in October. It is thought to spread another mutation seen on About 10,000 genomes a week this has given rise to thousands 4000 The evolution that has occurred Such an escape becomes even growth of case numbers in Kent faster too, but there is less B.1.1.7. However, it remains are sequenced in the UK and there of different lineages. For Number of virus variants with is therefore mostly just random more likely as we begin to exert in south-east England, noticed evidence than for B.1.1.7. unclear if any of these other are plans to up that to 20,000 by example, there are more than different versions of the spike genetic drift rather than being selection pressure on the virus that one variant, now known as Why these variants spread variants also spread faster. March. The country also has a new 4000 different versions of the protein for breaking into host cells the virus adapting. in the form of vaccines, natural B.1.1.7, was spreading faster faster is unclear (see page 11). B.1.1.7 and its ilk will body called the G2P-UK National spike protein that the virus uses But not entirely. In May 2020, a immunity and drugs. Mutants than others. The evidence that B.1.1.7 has 17 defining continue to change, so there is Virology Consortium to keep track to break into host cells and which new variant with a mutation called that can evade these interventions it is more transmissible is mutations, and B.1.351 has nine. a risk they could become even of new mutations and warn about is the target of most vaccines. D614G started circulating. It seems could slip through the net growing ever stronger. The overall number of mutations more dangerous. The more potentially dangerous ones. Intriguingly, most of the 10,000 to be slightly more transmissible and start circulating wildly, This variant is spreading faster isn’t unusual and many of them people they infect, the more “Even though this virus is mutations seem to be induced by Estimated number of coronavirus than the original virus because potentially pushing us back than different variants in other have been found before. chances there are for these evolving slowly, we do really have the human immune system rather genomes sequenced every week of an alteration to its spike protein. towards square one in our regions of the UK and in at least There has been much focus viruses to evolve further. to take surveillance very, very than by RNA replication errors. in the UK About 90 per cent of the viruses efforts to beat the pandemic. three other countries: Ireland, on the only mutation common Michael Le Page seriously,” says Robertson. ❚

8 | New Scientist | 23 January 2021 23 January 2021 | New Scientist | 9 News Coronavirus

Immunisation International spread Will vaccines work on new variants? The global threat of the Some coronavirus variants seem able to partly dodge the immune system, coronavirus variants but there is still hope for our vaccines, reports Michael Le Page Michael Le Page

SOON after vaccination began in response only requires the THE more infectious coronavirus end of the first wave of infections, The B.1.1.7 variant is now many countries, reports of faster- recognition of viral proteins, variant from the UK has gone it would mean 128 deaths. spreading locally in other nations spreading coronavirus variants rather than the blocking of their global, causing fears that it could With a variant that is 50 per in Europe and in some US states. triggered fears that vaccines might function. This means it is harder lead to a new wave of infections cent more deadly, those 16,000 Given that the US is already not protect against them. The for resistance to evolve because and deaths around the world in cases would result in 192 deaths. hard hit and unlikely to use good news is that initial studies no single site is crucial. coming months if not brought But with a variant that is 50 per lockdown‑type measures, Angela suggest that the existing shots The T-cell response to the under control. That brings new cent more transmissible, though Rasmussen at Georgetown will still work, although they might coronavirus is broad, involving urgency to vaccination efforts. no more deadly, there would be University in Washington DC be slightly less effective against many parts of the spike protein The B.1.1.7 variant has so far 122,000 cases after a month, says this is a big worry. “When two variants, one that emerged in as well as other proteins. “There is been reported in 55 countries. leading to 976 deaths. you already have uncontrolled South Africa and one from Brazil. no way these variants are escaping There is no evidence that it is transmission and then you add “I am optimistic that current T-cell immunity,” says Crotty. more deadly, nor that it is yet another variant that is more vaccines will remain quite Unfortunately, while T-cells can spreading locally outside Europe 55 transmissible, you are going useful,” says Jesse Bloom at the stop people getting symptoms, and North America. But initial The number of countries with push the healthcare system Fred Hutchinson Cancer Research they cannot prevent infections. studies suggest that it is around reported cases of the UK variant past its limit,” she says. Center in Seattle. “But I do expect The bottom line is that existing 50 per cent more transmissible. Elsewhere in the world, most that eventually it will be necessary vaccines should still protect That is actually a bigger To halt a surge in UK cases reported cases of B.1.1.7 are in to update vaccines to account against B.1.351 and P.1, but might problem than if it were more partly due to B.1.1.7, England travellers, says Áine O’Toole at for viral evolution.” be slightly less effective. And there deadly, says Adam Kucharski and Scotland this month joined the University of Edinburgh, UK. Antibodies are our main is a danger of these variants or at the London School of Hygiene Wales and Northern Ireland in That means it may not yet be defence against viruses. When we others evolving to be much better & Tropical Medicine. strict lockdown. By the start of circulating locally and there might get infected by a new virus, our at evading protection. A simple calculation illustrates this week, all parts of the UK had be time to keep it out, she says. immune system starts producing why. Suppose 10,000 people are brought in tougher travel rules. Yet many countries may

NELSON ALMEIDA/AFP VIA GETTY IMAGES infected in a city and each infects Last month, Ireland began a be finding the variant only in a range of antibodies that bind Escape variants to various parts of viral proteins. 1.1 other people on average, the strict lockdown after reporting travellers because they aren’t Not all antibodies are equal. Production of the protection, says Bloom. The There have been reports of This means we need to step up low end for the estimated rate the fastest growth rate of any doing genetic sequencing for Studies show that only a few Sinovac vaccine in Brazil, antibodies might not be as reinfections in South Africa, Salim surveillance so we can spot any of in England now. country in coronavirus cases. local cases, says O’Toole. Most antibodies can “neutralise” with roll-out imminent effective, but they still get the job Abdool Karim, an epidemiologist such “escape variants” early and After a month, 16,000 people One reason was relaxed countries did little sequencing viruses and prevent infections. done. There were also differences advising the nation’s government, have time to update vaccines, says would have been infected. If the restrictions in early December, until recently, so B.1.1.7 could be These neutralising antibodies called E484. The variant from between individuals: antibodies said in an online presentation. Angela Rasmussen at Georgetown infection fatality rate is 0.8 per with pubs and restaurants spreading undetected in places. bind to key sites on viral proteins. Brazil, known as P.1, has almost from some worked just as well. There has also been a report of University in Washington DC. cent, as it was in England at the reopening, says Kingston Mills at The spread of the B.1.351 For the coronavirus, one such the same three mutations. More evidence comes from a woman in Brazil having more “It is unlikely that, overnight, Trinity College Dublin. But by last variant from South Africa appears site is the part of its so-called spike According to a computer model, a study by Rino Rappuoli at severe symptoms the second time a variant is going to emerge that Efforts are under way week, nearly half of all new cases more limited. Though more than protein that binds to receptors on B.1.351’s spread can be explained GlaxoSmithKline Vaccines in . round. But such reports are to be is capable of completely evading to contain a new variant were due to B.1.1.7. “I think it was a dozen countries have reported human cells and helps the virus by this variant being 50 per cent When his team grew the virus in expected, said Karim, and in South the vaccine,” she says. “But if we in Pretoria, South Africa a combination of both,” he says. cases, it is only known to be get inside – the receptor binding more transmissible or 20 per cent the presence of antibodies from a Africa there is no evidence of a are not looking, then we might transmitting locally in Botswana, domain. If this part of the spike better at evading immunity in systematic rise in reinfections. not find them until it’s too late.” Zambia and the UK, says O’Toole. protein changes, neutralising previously infected people, when “A mutation in the variants This could be because testing Scientists are already looking The similar P.1 variant that antibodies may not bind as well. compared with previous variants. from Brazil and South how well antibodies neutralise at how to update the vaccines and originated in Brazil has only been A rapidly spreading variant Lab studies point to the latter. Africa may help the virus viruses outside the body doesn’t it will be relatively easy to update found in travellers in Japan so far. named B.1.1.7, first spotted in Bloom and his team have tested evade antibodies” tell the whole story. The so-called most of them. The main delay These variants might be the UK, has only one mutation how mutations in the binding T-cell response is also important. could be getting them approved. dominating in South Africa and that affects this binding domain. domain alter the effectiveness previously infected person, E484K T-cells spot an infected cell New Scientist asked regulators Brazil because they seem slightly Initial studies of antibodies from of antibodies from people who was one of three mutations that by detecting viral proteins on in the UK, US and Europe what better at evading the immune those previously infected by the have been infected with the let the virus become resistant. its surface, and then destroy it manufacturers would need to do. response in previously infected coronavirus or given the Pfizer and coronavirus. Mutations at the These findings suggest that the before it releases more viruses. None has yet decided on the people and these countries have BioNTech vaccine show little or no E484 site made the biggest spread of B.1.351 and P.1 is due to “T-cells can be incredibly process, but some pointed to the had high levels of infections, says drop in effectiveness against B.1.1.7. difference, with neutralising the E484K mutation helping the valuable at preventing disease,” updating of seasonal flu vaccines Rino Rappuoli at GlaxoSmithKline The variant from South Africa, activity falling as much as tenfold. virus evade antibodies and says Shane Crotty at the La Jolla as a possible precedent. Updated Vaccines in Italy. If so, the variants called B.1.351, is of more concern. While that sounds alarming, reinfect people who have already Institute for in flu vaccines don’t have to undergo will have no transmission It has three mutations in the current vaccines work so well that had covid-19. “Whether on top California. “They can do it so well clinical trials, so the process could advantage in countries with low binding domain, including one even a big drop in neutralisation of this they are more infectious, that the person never gets sick.” be rapid. “I believe it can be done levels of immunity. But this will named E484K as it occurs at a site might not substantially reduce I don’t know,” says Rappuoli. Crucially, an effective T-cell very quickly,” says Rappuoli. ❚ PHILL MAGAKOE/AFP VIA GETTY IMAGES alter as vaccination ramps up. ❚

10 | New Scientist | 23 January 2021 23 January 2021 | New Scientist | 11 News Coronavirus Health Check newsletter Get a weekly round-up of health news in your inbox newscientist.com/healthcheck The long view The coronavirus could end up mild like a common cold Anthony King

POLICY-MAKERS are scrabbling encounters increasing resistance People at a supermarket in reoccur. A 1990 experiment in older people,” says Lavine. “As to contain the spread of the from antibodies among people Germany using face masks revealed that adults infected with primary infections increasingly coronavirus, as more highly who have been infected or to protect against covid-19 229E were open to reinfection one are restricted to children, we transmissible variants travel vaccinated, new mutations year later. The China CDC antibody expect the disease severity around the world. Yet the become more likely to take hold. (immunoglobulin M, or IgM) study also found that 70 per cent to overall become mild.” evolution of SARS-CoV-2 in this Indeed, some experts suggest that were found only in children. of adults had antibodies for the way comes as no surprise to the new variants we currently see Becoming a “common cold” is as four endemic coronaviruses. Unknown timescale virologists. In fact, it is probably arose inside the bodies of people much about us as the virus, says Every two to three years, it seems just one step on a much longer with long-lasting infections. Baric. “My guess is that many of people become more susceptible This has all happened before, evolutionary trajectory. In time, Lab studies back up this idea. these common coronaviruses, to these viruses, says Baric. They according to Van Ranst, who in virologists predict, the virus will “Some of these variants emerged if introduced directly into a very, are re-infected, but retain enough 2005 reported that OC43 probably become more benign, following in vitro when the virus was very naive population of adults, immune memory to fight off jumped to people from cattle and an evolutionary pathway cultured for several days in would probably be pretty brutal.” severe disease and experience triggered a pandemic in the late previously taken by four other the presence of convalescent Baric believes that as SARS- only mild symptoms. Reinfection 19th century dubbed the Russian human coronaviruses that today plasma,” says Manuela Sironi, CoV-2 bumps into more resistance seems to act as an immune booster. flu. The bad news is that we don’t cause nothing more than the an evolutionary virologist at the in adults, it may be pushed to know how long it took OC43 to “common cold”. How could Scientific Institute IRCCS Eugenio evolve in this direction. “It is dilute to a common cold virus this happen, and how will Medea in Italy. possible the virus has to change 4 or when SARS-CoV-2 will join our actions play a part? We don’t know exactly what a little just to maintain itself in Endemic coronaviruses the endemic club. “Our model Coronaviruses tend to evolve mutations might increase the children,” he says. It may evolve cause the common cold suggests that the quicker people slowly compared with other RNA speed at which the virus can to escape immunity by being able get exposed, the quicker we get viruses because they proofread spread. SARS-CoV-2 has four main to better replicate in the nose, and “Even without relevant genetic to that mild state,” says Lavine. their genetic material as they structural proteins, including the IMAGES ALVAREZ/GETTY LUIS so turn into an upper respiratory changes, SARS-CoV-2 might Without vaccines, that would replicate, so can filter out spike protein that sticks out from infection, like the other endemic eventually turn into the fifth push up deaths. mutations. What’s more, SARS- its surface and helps it attach to is more casino than science at the not to kill us or make us sick,” If so, we, as hosts, will be a coronaviruses. These occasionally endemic coronavirus,” says Sironi. What’s more, endemic CoV-2 isn’t currently under much cells in the body, as well as non- moment,” says Marc Van Ranst at he says. “The virus is successful crucial driver in this change. The cause serious disease in children, Recent modelling by coronaviruses can still cause pressure to change, says virologist structural proteins that hijack KU Leuven in Belgium. “There are when it is unnoticed and gets key here is that people never seem but usually result in little more epidemiologist Jennie Lavine pneumonia in older people. In Ralph Baric at the University of the machinery inside host cells. a gazillion possible mutations.” transmitted easily.” to first encounter these endemic than a runny nose. “Children at Emory University in Atlanta, 2003, when a disease ran rampant North Carolina at Chapel Hill. It Changes in transmission would Most virologists tend to agree, coronaviruses as adults. In 2013, typically have less severe disease Georgia, and her colleagues in an elderly care home in Canada is successfully colonising a new probably involve mutations in Familiar trajectory suspecting that SARS-CoV-2 will scientists at the Chinese Center for than adults,” says Baric. supports this, concluding that and killed one in 12 of the residents species – with an open banquet the spike, which is targeted by follow a similar evolutionary Disease Control and Prevention If SARS-CoV-2 follows once the virus is endemic and that it infected, a coronavirus of hosts – and variants that spread the vaccines, says Sironi. It is also difficult to predict trajectory to the four endemic (China CDC) in Beijing measured this pattern, then it should first exposure is in childhood, was suspected. It turned out to be faster are outcompeting others. It is impossible to say which whether SARS-CoV-2 will evolve to coronaviruses that cause the antibodies for these four common become much less deadly. Other SARS-CoV-2 will be relegated to a OC43. So even a much tamer SARS- But evolutionary pressures are mutations would make SARS- be more harmful, says Sironi. But “common cold”, prosaically called viruses. The type of antibodies coronavirus infections in healthy common cold. “Primary infections CoV-2 may still be a threat to older starting to kick in. As the virus CoV-2 more or less deadly. “That Van Ranst is optimistic. “Its aim is 229E, HKU1, NL63 and OC43. generated by a first infection adults are usually mild, but tend to be more severe, especially people for a long time to come. ❚

Covid-19 Early in the pandemic, infected especially with more transmissible This means that viruses – or While vaccines offer hope, 83 per cent for at least five months. Why eradication is unlikely people were infecting around variants. This could be hard to do. bacteria in the case of whooping they are no guarantee that the Even if we did manage to three others on average, leading Some covid-19 vaccines don’t reach cough – can circulate largely coronavirus will be eradicated eradicate the virus in humans, it VACCINE roll-out in a growing other viruses. “It does not seem to to estimates that two out of three this level of effectiveness when it undetected, popping up only might lurk in animals and jump back number of countries should be as mutable a virus as ,” people, or 67 per cent, need to be comes to preventing disease. when they spread to unvaccinated yet approved for people aged under into people later on. SARS-CoV-2 eventually allow life to return to says Mills. That means we shouldn’t immune to halt transmission. This What is more, it isn’t yet clear people and cause disease. 16, who make up a quarter of the can infect several other species, normal, but it is unlikely that we will need to update vaccines every year, is what we mean by herd immunity. to what extent any of the vaccines In other words, even vaccinating world’s population. including cats, dogs, ferrets, bats, be able to eradicate the coronavirus although occasional tweaks might Some people now think 70 to prevent transmissible infections, everyone on the planet might not However, we don’t have to rely hamsters, deers and tree shrews. that causes covid-19 altogether. be required. 90 per cent of the population may as opposed to merely preventing be enough to stop the coronavirus entirely on vaccines to achieve herd “I think this virus is here to stay,” “I don’t see that these vaccines will Despite this, wiping out the have to be immune to achieve this, symptoms, although this is still circulating at low levels, and we immunity. A study by Susan Hopkins says Hopkins, who points out that be eliminating SARS-CoV-2 any time virus will be really hard even if we being investigated. are unlikely to get close to this. at Public Health England and her the smallpox virus is the only one in the coming years,” says Kingston manage to vaccinate most people. “Even vaccinating A few vaccines, such as the In some countries many people colleagues suggests that natural we have managed to eradicate, and Mills at Trinity College Dublin. To stop a disease spreading, infected everyone on the one for , prevent say they will refuse the vaccine, infection with the coronavirus that took many years from the start Despite the many variants, the individuals must pass it on to less planet might not stop the symptoms, but don’t block such as France, where only 4 in 10 provides comparable protection, of the campaign to eliminate it. ❚

coronavirus mutates less than many than one other person on average. coronavirus circulating” transmission, says Mills. people want it. And no vaccine is IMAGES FURLONG/GETTY CHRISTOPHER reducing the risk of reinfection by Michael Le Page

12 | New Scientist | 23 January 2021 23 January 2021 | New Scientist | 13