Omicron has frightening mutations. That doesn’t mean they work well together

Omicron has frightening mutations.  That doesn’t mean they work well together

The Omicron variant of the coronavirus has alarmed many scientists about the sheer number of genetic mutations – around 50 total, including at least 26 that are unique to them. But more doesn’t necessarily mean worse: mutations sometimes work together to make a virus more terrifying, but they can also cancel each other out.

“In principle, mutations can also work against each other,” says Jesse Bloom, evolutionary biologist at the Fred Hutchinson Cancer Research Center in Seattle. “However, in this case the evolutionary selection tends to lead to the spread of a new variant with favorable than unfavorable mutation combinations.”

However, because of this phenomenon, known as epistasis, scientists hesitate to speculate on the properties of Omicron, although individual mutations in the variant are linked to greater transmissibility or the ability to evade the body’s immune defenses.

“It’s important to get a feel for the whole virus,” said Penny Moore, a virologist at the National Institute for Communicable Diseases in South Africa.

Dr. Moore’s team is among dozen around the world trying to understand whether current vaccines against Omicron will work. Researchers are creating artificial versions of the virus that contain all of Omicron’s mutations, rather than making judgments based on a subset of mutations.

This is what researchers learned last year when the beta variant appeared in South Africa. They estimated the ability of this variant to evade immunity based on a specific mutation, E484K. However, Beta also had two other mutations that affected vaccine sensitivity.

“The combination of these three mutations was more resistant than a virus that only contained E484K,” said Dr. Moors. The investigation of the individual mutation “turned out to be misleading”.

Omicron carries a mutation called N501Y that is believed to allow the virus to bind more closely to human cells. This mutation was also present in the alpha variant and was linked to its infection.

“Still, it was Delta that didn’t have that particular mutation that was even more transmissible than Alpha,” said Dr. Bloom. “That’s because Delta had other mutations that improve transferability.”

The infectivity of a variant depends on how well the virus binds to receptors on human cells, but also on the stability of the virus, where it replicates in the airways and how much of it is exhaled.

Omicron has a group of mutations, all of which are linked to closer ties to human cells. “But if they act together, they might have a slightly different effect,” said Dr. Bloom. For this reason, he cannot predict how the variant will behave in the body.

That requires laboratory studies that run around the world.

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Rachel Meadows

Rachel Meadows

Trending topics news writer who enjoys cooking, walking her dog and travel.

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