{"id":160327,"date":"2020-05-11T12:00:04","date_gmt":"2020-05-11T11:00:04","guid":{"rendered":"https:\/\/www.transcend.org\/tms\/?p=160327"},"modified":"2020-12-02T10:11:50","modified_gmt":"2020-12-02T10:11:50","slug":"the-problem-with-stories-about-dangerous-coronavirus-mutations","status":"publish","type":"post","link":"https:\/\/www.transcend.org\/tms\/2020\/05\/the-problem-with-stories-about-dangerous-coronavirus-mutations\/","title":{"rendered":"The Problem with Stories about Dangerous Coronavirus Mutations"},"content":{"rendered":"
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The Atlantic<\/em> is making vital coverage of the coronavirus. Find the collection here<\/a>.<\/strong><\/p>\n<\/section>\n

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There\u2019s no clear evidence that the pandemic virus has evolved into significantly different forms\u2014and there probably won\u2019t be for months.<\/em><\/p>\n<\/blockquote>\n

6 May 2020 –<\/em> As if the pandemic weren\u2019t bad enough, on April 30, a team led by scientists at Los Alamos National Laboratory released a paper<\/a> that purportedly described \u201cthe emergence of a more transmissible form\u201d of the new coronavirus, SARS-CoV-2. This new form, the team wrote, \u201cbegan spreading in Europe in early February.\u201d Whenever it appeared in a new place, including the U.S., it rapidly rose to dominance. Its success, the team suggested, is likely due to a single mutation, which is now \u201cof urgent concern.\u201d<\/p>\n

The paper has not yet been formally published or reviewed by other scientists. But on May 5, the Los Angeles Times<\/em> wrote about it<\/a>, claiming that \u201ca now-dominant strain of the coronavirus could be more contagious than [the] original.\u201d That story quickly went \u2026 well \u2026 viral.<\/p>\n

But \u201cthe conclusions are overblown,\u201d says Lisa Gralinski<\/a> of the University of North Carolina, who is one of the few scientists in the world who specializes in coronaviruses. \u201cTo say that you\u2019ve revealed the emergence of a more transmissible form of SARS-CoV-2 without ever actually testing it isn\u2019t the type of thing that makes me feel comfortable as a scientist.\u201d She and other virologists I\u2019ve spoken with who were not involved in the Los Alamos research agree that the paper\u2019s claims are plausible, but not justified by the evidence it presents. More important, they\u2019re not convinced different strains of the coronavirus exist at all.<\/p>\n<\/div>\n<\/div>\n

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\u201cWe have evidence for one strain,\u201d says Brian Wasik at Cornell University.<\/p>\n

\u201cI would say there\u2019s just one,\u201d says Nathan Grubaugh at Yale School of Medicine.<\/p>\n

\u201cI think the majority of people studying [coronavirus genetics] wouldn\u2019t recognize more than one strain right now,\u201d says Charlotte Houldcroft at the University of Cambridge.<\/p>\n

Everyone else might be reasonably puzzled, given that news stories have repeatedly claimed there are two<\/a>, or three<\/a>, or even eight<\/a> strains. This is yet another case of confusion<\/a> in a crisis that seems riddled with them. Here\u2019s how to make sense of it.<\/p>\n

Whenever a virus infects a host, it makes new copies of itself, and it starts by duplicating its genes. But this process is sloppy, and the duplicates end up with errors. These are called mutations\u2014they\u2019re the genetic equivalent of typos. In comic books and other science fiction, mutations are always dramatic and consequential. In the real world, they\u2019re a normal and usually mundane part of virology<\/a>. Viruses naturally and gradually accumulate mutations as they spread.<\/p>\n

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As an epidemic progresses, the virus family tree grows new branches and twigs\u2014new lineages that are characterized by differing sets of mutations. But a new lineage doesn\u2019t automatically count as a new strain. That term is usually reserved for a lineage that differs from its fellow viruses in significant ways. It might vary in how easily it spreads (transmissibility), its ability to cause disease (virulence), whether it is recognized by the immune system in the same way (antigenicity), or how vulnerable it is to medications (resistance). Some mutations affect these properties. Most do not, and are either silent or cosmetic. \u201cNot every mutation creates a different strain,\u201d says Grubaugh. (Think about dog breeds as equivalents of strains: A corgi is clearly different from a Great Dane, but a black-haired corgi is functionally the same as a brown-haired one, and wouldn\u2019t count as a separate breed.)<\/p>\n

There\u2019s no clear, fixed threshold for when a lineage suddenly counts as a strain. But the term has the same connotation in virology as it does colloquially\u2014it implies importance. Viruses change all the time; strains arise when they change in meaningful ways.<\/p>\n

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New strains of influenza arise every year. These viruses quickly acquire mutations<\/a> that change the shape of the proteins on their surface, making them invisible to the same immune cells that would have recognized and attacked their ancestors. These are clearly meaningful changes\u2014and they’re partly why the flu vaccine must be updated every year.<\/p>\n

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But influenza is notable for mutating quickly. Coronaviruses\u2014which, to be clear, belong to a completely separate family from influenza viruses\u2014change at a tenth of the speed<\/a>. The new one, SARS-CoV-2, is no exception. \u201cThere\u2019s nothing out of the ordinary here,\u201d says Grubaugh. Yes, the virus has picked up several mutations since it first jumped into humans in late 2019, but no more than scientists would have predicted. Yes, its family tree has branched into different lineages, but none seems materially different from the others. \u201cThis is still such a young epidemic that, given the slow mutation rate, it would be a surprise if we saw anything this soon,\u201d Houldcroft says.<\/p>\n<\/section>\n<\/div>\n<\/div>\n

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What of the Los Alamos study, then? The team, led by Bette Korber, looked at mutations that affect the virus\u2019s \u201cspike\u201d\u2014the protein on its surface that it uses to recognize host cells. One particular mutation, known as D614G, caught their attention. It changes just one of the many molecules that make up the spike, subtly altering the protein\u2019s shape. The viruses without this mutation\u2014the D lineage\u2014include the one that first emerged in Wuhan, China. The viruses with the mutation\u2014the G lineage\u2014appeared sometime in February. Worldwide, the G\u2019s were relatively uncommon in early March, but by April, they had become dominant in much of Europe, North America, and Australia.<\/p>\n

But this pattern is hard to interpret. The D614G mutation might make the coronavirus more transmissible, and G-viruses might have become more common because they outcompeted the D-viruses. But it\u2019s also possible that the mutation might do nothing, and G-viruses have become more common because of dumb luck.<\/p>\n

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If those viruses happened to be in the right people\u2014those who traveled from China to Italy before the latter went into lockdown\u2014they could easily have spread explosively across Europe, and eventually into the U.S<\/a>. Indeed, that\u2019s the pattern we see: The D614G mutation first appeared just before the coronavirus moved into Europe<\/a>, and almost all the G-viruses around today are descendants of that initial continent-hopping pioneer. China\u2019s intense social restrictions likely stamped out many other coronavirus lineages within its borders, and stopped them from spreading further. \u201cThe only lineages you\u2019ll see are those that got out, which include the ones with this mutation,\u201d says Bill Hanage of Harvard, who studies pathogen evolution.<\/p>\n

Such events are especially important in the early stages of a pandemic. Some virus lineages will do really well and others will disappear for reasons that have nothing to do with the viruses themselves and everything to do with the movements of their human hosts, whom those hosts interact with, and the policies enacted by the countries those hosts live in.<\/p>\n

This isn\u2019t to say that the Los Alamos study is bad or wrong\u2014it comes from a respected team and presents interesting data. But the evidence it provides cannot distinguish between two equally plausible explanations\u2014that the G-viruses were more transmissible, or that the G-viruses were just lucky. (Korber didn\u2019t respond to a request for an interview.)<\/p>\n

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More definitive evidence could take two forms. First, scientists could compare the spread of the epidemic among groups of people who were infected by the D- and G-viruses. But \u201cthat\u2019s a very difficult study to design,\u201d Houldcroft says. You\u2019d need to ensure that the two groups were closely matched, so that any differences between them were actually due to the virus. You\u2019d need both reliable clinical data and viral sequences from each person. And you\u2019d need to look at a lot of people\u2014and viruses\u2014to be confident the results weren\u2019t statistical flukes. \u201cI wouldn\u2019t put much weight on studies that had fewer than thousands of viral genomes, or tens of thousands,\u201d Houldcroft says. \u201cAnd we won\u2019t have those kinds of samples collected and analyzed for several months yet.\u201d<\/p>\n<\/section>\n<\/div>\n