The Coronavirus is Mutating. It’s Unclear if That’s a Problem.
Here’s what you should know
The novel coronavirus has mutated, and the mutated form of the virus now accounts for most cases in the U.S. and across the globe. That’s the major finding of a recent study, published July 3 in the journal Cell, which also found evidence that the mutated coronavirus may be more infectious than its predecessor.
“The first cases on the West Coast of the U.S. were the original type that emerged in China,” says Erica Ollmann Saphire, PhD, one of the authors of the new study and a professor at the La Jolla Institute for Immunology in California. “The new form came to the East Coast of the U.S. from Europe, and it’s now globally dominant.” Her study includes color coded graphs that reveal how the mutated virus appeared to wrest control from the older virus; in New York City, the mutated virus was dominant almost from the get-go.
The principal author of the new study, Bette Korber, PhD, says that the newer “variant” of the virus was first identified in Italy, and that it likely emerged from a mutation in a single individual. While the old virus persisted in some parts of the U.S., and may still be the most prevalent form in a few places, Korber, who is a research scientist at the U.S. Government’s Los Alamos National Laboratory, says that the new variant has made up the majority of cases in just about every U.S. sampling location since May.
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More research is needed to confirm this study’s finding that the new variant of the virus may be more transmissible — meaning more spreadable — than the older one. But Saphire says that both lab and clinical work in her group’s study indicate that the mutated virus creates more copies of itself and also produces a higher “viral load” in the people it infects, both of which could contribute to heightened spread. She also says that in places where both forms of the virus have circulated, the newer form usually “took over,” which suggests that it may have a fitness advantage over the original virus.
All of this has important implications for future research — including the development of treatments and vaccines. “It’s very clear we need to keep an eye on these mutations,” Saphire says.
Understanding the new virus
Viruses are living organisms. And like all living organisms, they have the ability to evolve — to acquire adaptations that increase their ability to survive and thrive.
These adaptations can be major or minor. In some cases, they can change a virus in ways that interfere with the actions of a vaccine. The influenza virus, for example, is genetically unstable and constantly evolving; this partly explains why each new flu season requires a new flu vaccine, and the efficacy of that new vaccine varies from year to year.
Compared to the flu virus, coronaviruses are relatively stable. Experts tend to view this stability as a good thing because it means that, if and when we have an effective SARS-CoV-2 vaccine, the virus is unlikely to mutate in ways that diminish that vaccine’s potency.
But Saphire says that the novel coronavirus is so prevalent — more than 13 million confirmed cases worldwide as of July 14, and a great many more unconfirmed cases — that even if mutations are statistically rare, they will emerge. She explains that most of these mutations “don’t go anywhere” — meaning they don’t confer any fitness advantage on the virus, and so they do not spread widely among people. But the mutations that her team identified are the rare exceptions. “The variant that has emerged has four changes in it, including one in the surface spike protein, which is the one we’re concerned about,” she says.
“People originally claimed that even if mutations happen, they wouldn’t have any effect on functionality. But clearly that’s not true.”
“Spike proteins” are those nubby protrusions that coat the outside of the virus, making it resemble a WWII-era water mine. Those spike proteins allow the virus to fuse with and invade healthy cells. Saphire says that they’re also a “major target” in the vaccines that are now in development. If a mutation causes changes to these spike proteins, she says, “one of the worries is that the antibodies might suffer.”
Antibodies are immune system proteins that can effectively block the virus’s ability to attach itself to healthy cells. If the virus changes in ways that render these antibodies ineffective, that’s bad news for several reasons. For one thing, it means that people who have already weathered a SARS-CoV-2 infection might not be protected from a second infection. It also means that vaccines, which are designed to make the immune system pump out protective antibodies, might not work as well — or at all. Saphire also says that prospective monoclonal antibody treatments, which involve injecting people with copies of virus-repelling proteins, could also be rendered ineffective by spike-protein mutations.
So far — and thank goodness — the dominant SARS-CoV-2 mutations don’t seem to interfere with the helpful action of antibodies. “This is a tremendous relief,” she says. Also, the new variant doesn’t seem to make people any sicker than the old one; some of Saphire’s colleagues performed an analysis of roughly 1,000 Covid-19 patients in Sheffield, England, and that analysis did not find evidence that the newer virus was associated with worse hospital outcomes.
But the mutations that her study examined emerged quickly — within a few months of the novel coronavirus’s initial identification in China. It’s a certainty that the virus will undergo more mutations — some of which may have already occurred. And these mutations may have wide-ranging effects.
What new mutations could bring
Since the start of the pandemic, virus experts have understood that the novel coronavirus would mutate. But the common assumption was that these mutations would be so minor as to be insignificant. “People originally claimed that even if mutations happen, they wouldn’t have any effect on functionality. But clearly that’s not true,” says Lee Riley, MD, a professor and chair of the Division of Infectious Diseases and Vaccinology at the University of California, Berkeley School of Public Health.
Like Saphire, Riley says that any mutations that stick are ones that will increase the virus’s “fitness,” and improved fitness could have good or bad ramifications for the human species. “It may become adapted in ways that help it spread even more efficiently, which may already have happened,” he says. That’s bad. On the other hand, the virus may also adapt in ways that render it less pathogenic — meaning the sickness it causes could become less severe. In fact, Riley says that this sort of illness-weakening “attenuation” is what normally happens to viruses as they mutate — the reason being that viruses that are too deadly tend to run out of hosts.
Stephen Morse, PhD, is a professor of epidemiology and infectious disease at Columbia University’s Mailman School of Public Health. He says that as viruses mutate in ways that increase their ability to spread — which, according to the new study, may have already occurred — this change tends to go hand in hand with a decrease in the virus’s lethality. “That’s what usually happens,” he says. (The recent and now nearly month-long surge in U.S. cases has thus far produced only a modest spike in deaths — though experts say that there are a lot of potential explanations for this that have nothing to do with the virus weakening.)
Saphire agrees that viruses often weaken over time. “As viruses adapt to human populations, they tend to get milder,” she says. But a tendency is not a certainty, and she says that there’s no knowing just what the novel coronavirus will do next. “Mutations are random events,” she adds.
She and countless other scientists will keep a close eye on the virus. But whether SARS-CoV-2’s evolution will be helpful or harmful to its human hosts remains an open question.