All viruses mutate and the corona virus is no exception. However, there is still no compelling evidence that it is developing in a way that has made it more contagious or deadly.
A preprint study – published online but not published in a scientific journal and not yet reviewed by experts – set the Internet on fire 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 occurred in February in Europe and then quickly spread and dominated as a virus was introduced to new countries.
The mutation, they wrote, “is urgent” because it made the corona virus more transmissible. After media coverage, the prospect of turbo-charged hopscotching has unsettled many people around the world who already had enough in mind.
However, experts in viral evolution are far from convinced. For one thing, there is no new strain: in contrast to the flu, the coronavirus has not yet been divided into clearly different forms.
It does mutate, but that’s exactly what viruses do. Just because a mutation occurs more often is not evidence that it changes the way the virus works.
Dr. Korber did not immediately respond to an email request for a comment.
Mutations are tiny changes in the genetic material that occur when copying. Human cells have many so-called proofreading proteins that rarely keep mutations. Still, every baby arrives with dozens of new genetic mutations.
Viruses are much sloppy and produce many mutants each time they infect a cell. Many of these mutations are not useful for the virus because they deactivate it rather than contribute to proliferation. Some can be beneficial for the virus. The rest have little effect in one way or another.
Natural selection can favor viruses that carry a beneficial mutation, resulting in a wider spread. But it is also possible that a neutral mutation just happens to occur more often, a process known as genetic drift.
“I don’t think they provide evidence of an improvement in portability,” Sergei Pond, an evolutionary biologist at Temple University, said in an email about the new report. “To determine this, you need direct competition between tribes in the same geographic area.”
In some of these cases, viruses carrying the mutation did not decrease in the population. Instead, the gene returned to its original form, suggesting that D614G did not give the virus any particular advantage.
Some researchers went to Twitter to criticize the paper. “I think these claims are suspect to say the least,” wrote Bill Hanage, epidemiologist at Harvard T.H. Chan School of Public Health.
“They got a bit over their skis in terms of titles and conclusions,” wrote Brian Wasik, an evolutionary biologist at Cornell University. “You deserve a strong and good faith assessment.”
None of the critics ruled out the possibility of a mutation that would make the virus more transmissible. And it is possible that D614G delivered some kind of border.
But it will take much more evidence to rule out other explanations.