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The Coronavirus Is Mutating. But That May Not Be A Problem For Humans

A colorized image of cells from a patient infected with the coronavirus SARS-CoV-2. The virus particles are colored pink. The image was captured from a scanning electron micrograph.
A colorized image of cells from a patient infected with the coronavirus SARS-CoV-2. The virus particles are colored pink. The image was captured from a scanning electron micrograph.

As the new coronavirus continues to spread around the globe, researchers say the virus is changing its genetic makeup slightly. But does that mean it is becoming more dangerous to humans? And what would the impact be on any future vaccines?

"In the literal sense of 'is it changing genetically,' the answer is absolutely yes," says Marc Lipsitch, an infectious disease epidemiologist at Harvard University. "What is in question is whether there's been any change that's important to the course of disease or the transmissibility or other things that we as humans care about."

So far, "there is no credible evidence of a change in the biology of the virus either for better or for worse," says Lipsitch.

Coronaviruses — like all viruses — change small parts of their genetic code all the time.

"Viruses mutate naturally as part of their life cycle," says Ewan Harrison, scientific project manager for the COVID-19 Genomics UK Consortium, a new project that tracks the virus in the United Kingdom.

Like flu and measles, the coronavirus is an RNA virus. It's a microscopic package of genetic instructions bundled in a protein shell. When a virus infects a person, the string of genetic instructions enables the virus to spread by telling it how to replicate once it enters a cell. The virus makes copies of itself and pushes them out to other cells in the body. Infectious doses of the virus can be coughed out in droplets and inhaled by others.

Inevitably, viruses "make mistakes in their genomes" as they copy themselves, says Harrison. Those changes can accumulate and carry over to future copies of the virus. Researchers are using these small, cumulative changes to trace the pathway of the virus through groups of people.

So far, researchers who are tracking the genetic changes in SARS-CoV-2 — the official name for the coronavirus — say it seems relatively stable. It acquires about two mutations a month during this process of spread, Harrison says — about one-third to one-half the rate of the flu.

Coronaviruses differ from flu viruses in another key way that reduces the number of mutations. They proofread their own genomes when they copy themselves, cutting out things that don't seem right. "They maintain this ability to keep their genome pretty much intact," says Vineet Menachery, a virologist at the University of Texas Medical Branch. "The mutations that they incorporate are relatively rare."

This added proofreading function means that coronaviruses are also one of the largest RNA viruses. They're about 30,000 nucleotides long — double the size of flu viruses. But at 125 nanometers wide, they're still microscopic; 800 of them could fit in the width of a human hair.

Nonetheless, their relatively larger size means "they have a lot more tools in their tool belt" compared with other RNA viruses, says Menachery — in other words, more capability of fighting off a host's immune system and making copies of themselves.

Researchers are on alert for changes that might affect how the coronavirus behaves in humans. For instance, if the coronavirus developed ways to block parts of our immune system, it could hide out in our bodies and establish itself better. If it evolved to bind more strongly to human cells, it could enter them more efficiently and replicate more quickly.

But it's not as if the coronavirus needs to become more potent to survive and thrive. It's already replicating itself around the world very successfully, says Justin Bahl, an evolutionary biologist at the University of Georgia. "The viruses themselves are not actually under much pressure to change."

Selective pressures could come from introducing treatments and vaccines that are effective against a narrow group of coronavirus strains. If that happens, strains that aren't targeted by these measures would likely proliferate.

The small genetic changes that researchers have observed so far don't appear to be changing the function of the virus. "I don't think we're going to see major new traits, but I do think that we're going to see different variants emerge in the population," says Bahl.

And that slower rate of change is potentially good news for treatments and vaccines. Researchers think that once a person gains immunity against SARS-CoV-2, either by recovering from an infection or by getting a future vaccine, they will likely be protected against the strains in circulation for "years rather than months," predicts Trevor Bedford, an evolutionary biologist at the Fred Hutchinson Cancer Research Center, in an assessment shared on Twitter.

Projects such as the COVID-19 Genomics UK Consortium will use these genetic drifts to track the path of the virus and figure out if there are hospitals or community hubs that are hot spots for contagion, according to Harrison. This will give public health officials a sense of where and how the virus is being transmitted now.

Will the coronavirus surge when schools reopen? Will new strains emerge that develop resistance to drugs or vaccines that are introduced? To answer such questions, Harrison says, the long-term plan is to track the virus in real time — and see how it changes as it spreads.

Copyright 2020 NPR. To see more, visit https://www.npr.org.