Now, 11 months later, the D614G mutation she helped identify is ubiquitous worldwide and appears in the genomes of the rapidly spreading variants in the United Kingdom, South Africa and Brazil. Meanwhile, new variants emerge in increasingly complicated patterns, leading leading biologists to look for other ways to track the enormous amount of genomic data received.
The goal: to quickly detect variants that can decrease the effectiveness of vaccines for a pathogen that is unlikely to be eradicated anytime soon. The SARS-CoV-2 virus may have come to stay and become a mere nuisance like the common cold. Or, like the flu, it may maintain its ability to cause serious illness in some segments of the population, a scenario that may require regular booster doses.
“By watching it carefully, we can get ahead of the virus and that’s what everyone is trying to do now,” said Korber, who works to create mathematical tools to detect medically significant variants.
The flood of new data from the genome is so great that the Los Álamos laboratory had to update its servers to process the information received. Meanwhile, Korber takes part in four weekly calls by Zoom with global experts to define criteria and decide when the mutations are worrying enough to warrant detailed laboratory follow-up on how they can affect vaccines.
A mystery investigated from the beginning by scientists is what type of virus the coronavirus will turn into. So far, it looks more like the flu virus, which changes shape all the time and requires annual vaccination, than with measles, a virus so intolerant of the mutation that a vaccine regimen lasts a lifetime.
“Does this mean that we need to produce a new vaccine every year?” said Paul Duprex, who heads the University of Pittsburgh’s Vaccine Research Center. “We do not know.”
The HIV virus is known for its rapid rate of mutation. In comparison, SARS-CoV-2 mutates at a much slower rate, in part due to an enzyme that limits changes. But, with more than 125 million infections worldwide, some errors can escape.
At the same time, the virus has found tortuous ways that can prevent its reading mechanism, researchers at the University of Pittsburgh found. Rather than making changes to individual letters of RNA, it excludes groups of several letters at once, apparently diminishing the ability of natural virus scanning systems to see the change.
What makes the future of SARS-CoV-2 so difficult to predict is that viral evolution is like a three-dimensional game of chess. It is not just individual mutations that matter, but also the order and combinations in which they occur. A single mutation can alter the virus in subtle ways that change the impact of others in the future, according to Mark Zeller, a scientist at the Scripps Research Institute in San Diego.
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