Where did the coronavirus omicron variant come from? Scientists suggest it evolved in one person.
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Charles Darwin could have learned a thing or two about evolution from the SARS-CoV-2 virus.
As it has passed back and forth across the world over the past two years, the pandemic-causing virus has changed, sometimes bit by bit; in the case of the omicron variant, seemingly in many ways at one time.
Scientists say these changes can be explained by how the coronavirus works, and how infecting people can drive mutations.
Unlike some viruses, the SARS-CoV-2 virus that causes COVID-19 has a self-correcting mechanism – like spell-check – fixing some of the random mistakes it makes as it copies itself. The coronavirus typically only changes about 2 of the 30,000 letters in its genome a month as it transmits from person to person.
But when someone with a weakened immune system tries to control the virus, it can shape-shift to avoid its own destruction.
Studies have shown that people in treatment for cancer, immunosuppressed after an organ transplant or weakened by HIV can remain infected with COVID-19 for months, while the coronavirus accumulates changes that make it harder to wipe out.
No “patient zero” has been found for omicron or any other variant, but scientists think they likely evolved within a single immunocompromised person.
“It’s reasonable speculation, but we don’t know for sure,” said Jesse Bloom, who studies viral evolution at the Fred Hutchinson Cancer Research Center in Seattle.
Omicron has 50 spelling changes from the original version of the virus, including 30 on the spike proteins that sit on the surface of the virus and are the target of vaccines and some treatments.
Those changes didn’t evolve one at a time as the virus passed from one person to another, surveillance data suggests, but seem to have arrived together – lending support to the idea that they co-evolved within a single person.
Experts say it’s too soon to know whether all those changes will make the variant less subject to protection from vaccines and previous infections, or whether it will be able to evade monoclonal antibody treatments.
For one variant to take over, it has to beat out others, either by transmitting more effectively or by being able to make more copies of itself once it reaches a new host.
“If it transmits well but doesn’t replicate well in its new host, it’s not as likely to win out in the end, because it’s got a dead-end path,” said Dr. Bruce Walker, an immunology professor at Harvard Medical School and the Massachusetts Institute of Technology.
Mutations that offer a survival advantage “can get into more people and create more viruses to infect more of the species,” he said.
In a normal person, whose immune system clears the virus in about a week, there’s not much time for mutations to accumulate, said Walker, also director of the Ragon Institute of MGH, MIT, and Harvard, an interdisciplinary immune research center.
But in an immunocompromised person, the virus might linger for months, studies show.
News source : Karen Weintraub, USA TODAY
