Editor's Note (12/30/20): Today health officials in Colorado confirmed the first case of a new mutated form of SARS-CoV-2 in the U.S., and said the state had a potential second case as well. Scientists, as noted in our story below, continue to find evidence this new variant appears more transmissible than the original form. Yet it does not appear to cause more severe disease. And the newly-authorized vaccines seem very effective against it.
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 17 mutations 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 17 new 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.
The mutations may not help this version of the SARS-CoV-2 virus evade all of the cells and proteins that our immune systems use to neutralize it. Initial data from the lab of Vineet Menachery, a microbiologist at UTMB, suggest that the N501Y variant is just as susceptible to our defenses as the original virus. But these genetic alterations might spell bad news for monoclonal antibody treatments against the virus. A December 1 preprint study found that the mutations drove changes to a segment of virus that lies very close to the regions recognized by monoclonals made by the pharmaceutical companies Eli Lilly and Regeneron, making it more difficult for the antibodies to bind and neutralize the pathogen.
The most pressing question, Farzan and others say, may be how the new variant will affect existing COVID-19 vaccines and the development of new ones. It does not appear that B.1.1.7 can resist the authorized vaccines developed by Pfizer and Moderna, respectively, or those made by other companies that are still being tested. Still, the fact that mutations are accumulating in the spike protein could mean that vaccines may, after an extended period of time, become somewhat less effective. That problem would force vaccine developers to adapt their products to ensure they can target new versions of the virus. “A lot of people think this is going to be like flu, with a new vaccine every year,” Weaver says.
He and others say that mutations in the virus are no reason for people to skip one of the vaccines because they are still very effective. They protect more than 90 percent of people against COVID illness. And there have been no signs in clinical trials that the virus—including any new variants—is resisting vaccination efforts.
The new U.K. mutant does makes it even more important for people to use public health measures such as physical distancing and mask wearing, Racaniello says. These strategies will slow down the spread. “While the vaccines should still work, we’re at even more risk of overwhelming our hospitals and health care workers,” says epidemiologist Lisa Gralinski of the University of North Carolina at Chapel Hill. “We’re already pretty stretched thin in health care in the U.S. The last thing we need is more cases coming in more quickly.”
Like Fauci, Gralinski says the variant is probably already in the U.S. She says the U.K. likely detected the mutation first because of its strong viral surveillance program—the nation tries to analyze genetic sequences of 10 percent of all cases and compare them to spot any changes. The U.S., by contrast, has no such centralized effort. “We’re flying a little bit blind right now,” Gralinski says. “We have to assume the variant is here.”
Mokdad’s group and others are now working over the December holidays to sequence existing U.S. samples of the virus. A more transmissible variant might explain, for instance, the recent spike in cases in California. Health officials could have missed the new version, he says, and assumed that the rapid rise in COVID-19 cases occurred because of increased travel around Thanksgiving. “It’s a wake-up call for all of us to find out as early as possible in order to make sure we know what’s circulating—especially how it will impact the vaccine,” Mokdad says. “It’s a race against time.”