A new mutated form of the novel coronavirus that appears more transmissible than the original has raised alarm in the U.K. and around the world. It does not appear to cause more severe disease, and the newly available vaccines do seem to protect people against it. Yet on December 19—after an announcement that the variant, dubbed B.1.1.7, had suddenly accumulated 17mutations and was spreading rapidly in the U.K.—the nation’s prime minister Boris Johnson announced stricter lockdowns there. And numerous European countries have halted travel from that nation.

The response from the U.S. has been mixed, with political figures such as New York State governor Andrew Cuomo first calling for suspending airline flights from the U.K., then shifting to ask for mandatory testing of travelers. But scientists such as Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, say that flight bans are probably too late to stop the variant spreading to the U.S. “I would not be surprised at all if it is already here,” he told Good Morning America on December 22.

Based on mathematical models, calculations by the COVID-19 Genomics UK consortium suggest that B.1.1.7 might be up to 70 percent more transmissible than the original virus. “It’s a shocking valuation, clearly something new that’s circulating,” says Ali Mokdad, a population health expert at the University of Washington. “Any mutation out there is a concern for us. This is a stubborn and opportunistic virus.”

Some researchers, however, doubt that the rapid spread of the new variant in the U.K. necessarily means it is more transmissible. “I do agree we should look into these things. But until we have some data, we should really be careful about what we say,” says Vincent Racaniello, a virologist at Columbia University. The best information on transmissibility will come from studies of animals that look at whether this variant moves more easily from one creature to another, and that work has not yet been published. Because the majority of COVID-19 outbreaks are caused by superspreaders, Racaniello says, it is conceivable that one person or a few individuals spread the new variant widely.

But others disagree. In the U.K., the variant has been increasing steadily over time, not suddenly as would be expected following a superspreader event, says Scott Weaver, an immunologist at the University of Texas Medical Branch (UTMB).

Furthermore, eight of the B.1.1.7 variant’s 17new mutations are on the spike protein: the portion of the coronavirus’s shell that allows it to bind to receptors on cell surfaces and infect cells. One of the spike protein mutations, called N501Y, appears in another new variant from South Africa and seems to improve the virus’s binding ability. Better binding could, in theory, lead to more transmission.

Michael Farzan, an immunologist at the Scripps Research Institute, says that the fact that the N501Y mutation appears to have appeared independently several times in different geographical areas is further evidence that it does give the virus some sort of advantage. Other spike protein mutations, including one called D614G that has been seen in the U.S., allow the virus to replicate better in the upper respiratory tract of mice rather than the lower tract. This arrangement could allow the virus to more easily spread through sneezing and coughing. The D614G variant has been circulating for some time, however, and it has not been shown to be more infectious in people or to create more serious symptoms.

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