Less than 2 weeks later, that variant is causing mayhem in the United Kingdom and elsewhere in Europe. Yesterday, U.K. Prime Minister Boris Johnson announced stricter lockdown measures, saying the strain, which goes by the name B.1.1.7, appears to be better at spreading between people. The news led many Londoners to leave the city today, before the new rules take effect, causing overcrowded railway stations. The Netherlands, Belgium, and Italy announced they were temporarily halting passenger flights from the United Kingdom. The Eurostar train between Brussels and London will stop running tonight at midnight, for at least 24 hours.
Scientists, meanwhile, are hard at work trying to figure out whether B.1.1.7 is really more adept at human-to-human transmission—not everyone is convinced yet—and if so, why. They’re also wondering how it evolved so fast. B.1.1.7 has acquired 17 mutations all at once, a feat never seen before. “There's now a frantic push to try and characterize some of these mutations in the lab,” says Andrew Rambaut, a molecular evolutionary biologist at the University of Edinburgh.
Too many unknowns
Researchers have watched SARS-CoV-2 evolve in real time more closely than any other virus in history. So far, it has accumulated mutations at a rate of about one to two changes per month. That means many of the genomes sequenced today differ at about 20 points from the earliest genomes sequenced in China in January, but many variants with fewer changes are also circulating. “Because we have very dense surveillance of genomes, you can almost see every step,” Loman says.
But scientists have never seen the virus acquire more than a dozen mutations seemingly at once. They think it happened during a long infection of a single patient that allowed SARS-CoV-2 to go through an extended period of fast evolution, with multiple variants competing for advantage.
One reason to be concerned, Rambaut says, is that among the 17 mutations are eight in the gene that encodes the spike protein on the viral surface, two of which are particularly worrisome. One, called N501Y, has previously been shown to increase how tightly the protein binds to the angiotensin-converting enzyme 2 receptor, its entry point into human cells. The other, named 69-70del, leads to the loss of two amino acids in the spike protein and has been found in viruses that eluded the immune response in some immunocompromised patients. (...)
In a press conference on Saturday, chief science adviser Patrick Vallance said that B.1.1.7, which first appeared in a virus isolated on 20 September, accounted for about 26% of cases in mid-November. “By the week commencing the ninth of December, these figures were much higher,” he said. “So, in London, over 60% of all the cases were the new variant.” Johnson added that the slew of mutations may have increased the virus’s transmissibility by 70%.
by Kai Kupferschmidt, Science | Read more:
Image: Stefan Rousseau/PA via AP Images
[ed. Uh, oh. See also: here and here (Bloomberg). Also: How The Hell Do We Deal With The Virus Mutating? (Sergey Alexashenko, Substack; and, What We Know About The New U.K. Variant Of Coronavirus — And What We Need To Find Out (NPR).]