Covid-19 Mutated. Can Vaccines Keep Up?

Covid-19 Mutated. Can Vaccines Keep Up?

One of the factors that will drive the future of the Covid-19 pandemic is how the virus evolves. And last week, scientists announced the first evidence that the virus has evolved to be more transmissible.

The mutation happened around late February, as the virus moved from East Asia to Europe. The first group to publish a paper raising this possibility was led by computational biologist and HIV evolution expert Bette Korber at Los Alamos National Laboratory. She couldn’t quite convince the scientific community, but virologist Ralph Baric of the University of North Carolina was persuaded enough to continue this line of investigation. Last week, after a series of experiments in cells and hamsters, he and Yoshihiro Kawaoka at the University of Wisconsin published a more complete case in Science. The implications for the history of the virus and its likely future are profound.

Natural selection favors organisms that are better at survival and reproduction. For viruses like Sars-CoV-2, that means reproducing prolifically and transmitting to new hosts easily. So far, scientists have found only one mutation that improves the survival ability of the virus. The more transmissible strain is referred to as G614, and the ancestral one as D614. It doesn’t look like the G strain is any deadlier than the D. Being deadlier might actually make a virus less evolutionarily fit, because viruses die with their hosts.

The other good news, says Baric, is that the structure of the spike proteins on the now-dominant G strain make it more vulnerable to being wiped out by vaccine-induced antibodies. That’s true even though the vaccines were all developed to work against the ancestral D strain. And G is probably more vulnerable to antibodies from past infections as well.

To test G’s transmissibility, they started with cultured cells that mimic cells from the nasal passages down to the deepest parts of the lung. Then they genetically manipulated the D strain, adding just the one mutation that Korber thought gave the G strain an edge. And indeed, the mutation did allow the virus to spread from cell to cell better than the original. They also infected the same cells with both viral strains and found the mutant strain dominated, over and over.

That may have been how it all started — with the mutation cropping up in a human host, becoming dominant in the airways of that person, and spreading to other people in a chain of transmission that crossed continents.

To test the possibility that the mutant strain is more contagious, the researchers also used hamsters housed in separate cages. They found viruses with the mutation were much more likely to travel through the air from infected hamsters in one cage to uninfected ones in another.

That mutation in the G strain may explain why the virus became so explosive once it got to Europe, and why, while early U.S. outbreaks were traced to China, the bulk of U.S. infections have now been traced to Europe. Even the predominant strain in Southern California came not from Asia but from Europe via New York. The D strain is still around, but it makes up about 2% of infections worldwide. Baric says there are reasons the G strain didn’t explode in China — mostly to do with the country’s much more Draconian lockdown policies as well as a system set up to support people who have to miss work if they need to quarantine.

Will the G strain find a way to evolve resistance to vaccines? It’s possible, Baric says. Once immunity builds up, the virus will be under pressure to change. As time goes on and more people develop immunity, evolution favors the viruses that are best at evading antibodies.

One way it could do that is to jump to another species, where it can evolve rapidly — as in Denmark’s minks, as Bloomberg Opinion colleague Sam Fazeli writes. Another concern is the possibility that the virus could jump to one of the world’s 1,400 bat species. Bats are good hosts for coronaviruses, and it’s still thought they were the most likely source of SARS-CoV-2.

That’s where the danger lies, Baric says. If the virus changes what he calls its antigenic structure, our antibodies might not recognize it.

But it’s also likely that this virus will do what other coronaviruses have done and become another common cold. Vaccine- and infection-induced immunity will likely protect people from the virus infiltrating the lower respiratory tract and beyond, but it might not protect everyone from getting a sniffly infection confined to the upper respiratory tract.

It would then join the four common coronaviruses already circulating among humans, all of which cause colds. Those viruses may have started off as deadly pandemics; one appears to have spread right around 1890, when there was a deadly pandemic known as Russian flu.

“Remember the virus really doesn’t want to kill anybody,” Baric says. “It just wants to replicate and transmit … so if it can manage to do that and take advantage of your nose as a major site for replication and transmission, then it’s happy as a lark because it’s surviving.”

If the vaccines work as well as hoped and the virus becomes the sniffles, we should feel the same way.

This column does not necessarily reflect the opinion of the editorial board or Bloomberg LP and its owners.

Faye Flam is a Bloomberg Opinion columnist. She has written for the Economist, the New York Times, the Washington Post, Psychology Today, Science and other publications. She has a degree in geophysics from the California Institute of Technology.

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