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“We have evidence for one strain,” says Brian Wasik at Cornell University.
“I would say there’s just one,” says Nathan Grubaugh at Yale School of Medicine.
“I think the majority of people studying [coronavirus genetics] wouldn’t recognize more than one strain right now,” says Charlotte Houldcroft at the University of Cambridge.
Everyone else might be reasonably puzzled, given that news stories have repeatedly claimed there are two, or three, or even eight strains. This is yet another case of confusion in a crisis that seems riddled with them. Here’s how to make sense of it.
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—they’re the genetic equivalent of typos. In comic books and other science fiction, mutations are always dramatic and consequential. In the real world, they’re a normal and usually mundane part of virology. Viruses naturally and gradually accumulate mutations as they spread.
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As an epidemic progresses, the virus family tree grows new branches and twigs—new lineages that are characterized by differing sets of mutations. But a new lineage doesn’t 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. “Not every mutation creates a different strain,” 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’t count as a separate breed.)
There’s 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—it implies importance. Viruses change all the time; strains arise when they change in meaningful ways.
New strains of influenza arise every year. These viruses quickly acquire mutations 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—and they’re partly why the flu vaccine must be updated every year.
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But influenza is notable for mutating quickly. Coronaviruses—which, to be clear, belong to a completely separate family from influenza viruses—change at a tenth of the speed. The new one, SARS-CoV-2, is no exception. “There’s nothing out of the ordinary here,” 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. “This is still such a young epidemic that, given the slow mutation rate, it would be a surprise if we saw anything this soon,” Houldcroft says.