All viruses mutate, and the coronavirus is no exception. But there is no compelling evidence yet that it is evolving in a way that has made it more contagious or more deadly.
A preprint study — posted online, but not published in a scientific journal and not yet peer-reviewed — has set the internet afire by suggesting otherwise.
On April 30, a report by a team led by Bette Korber, a biologist at Los Alamos National Laboratory in New Mexico, claimed to have found a mutation in the coronavirus that arose in Europe in February and then rapidly spread, becoming dominant as the virus was introduced into new countries.
The mutation, they wrote, “is of urgent concern,” because it made the coronavirus more transmissible. Following media coverage, the prospect of a turbocharged strain hopscotching around the world has unnerved many people who already had enough on their minds.
But experts in viral evolution are far from convinced. For one thing, there is no new strain: Unlike the flu, the coronavirus so far has not split into clearly distinct forms.
It does mutate, but that’s what viruses do. Just because a mutation becomes more common isn’t proof that it is altering how the virus functions.
Dr. Korber did not immediately respond to an email request for comment.
Mutations are tiny changes to genetic material that occur as it is copied. Human cells have many so-called proofreading proteins that keep mutations rare. Still, each baby arrives with dozens of new genetic mutations.
Viruses are far sloppier, producing many mutants every time they infect a cell. Many of these mutations aren’t useful to the virus, disabling it rather than helping it proliferate. A few may be beneficial to the virus. The rest have little effect one way or the other.
Natural selection can favor viruses carrying a beneficial mutation, leading it to spread more widely. But it’s also possible for a neutral mutation to become more common simply by chance, a process known as genetic drift.
“I don’t think they provide evidence to claim transmissibility enhancement,” Sergei Pond, an evolutionary biologist at Temple University, said of the new report in an email. “In order to establish this, you’d need direct competition between strains in the same geographic area.”
On some of those occasions, viruses carrying the mutation didn’t take off in the population. Instead, the gene reverted to its original form, suggesting that D614G didn’t give the virus any special advantage.
Some researchers took to Twitter to critique the paper. “I think those claims are suspect, to say the least,” wrote Bill Hanage, an epidemiologist at the Harvard T.H. Chan School of Public Health.
“They got a bit over their skis on title, conclusions,” wrote Brian Wasik, an evolutionary biologist at Cornell University. “They deserve a strong and good-faith peer review.”
None of the critics ruled out the possibility that a mutation could arise that would make the virus more transmissible. And it’s possible that D614G has provided some sort of edge.
But it will take much more evidence to rule out other explanations.