Because an immunocompromised host does not produce many antibodies, many viruses must spread. And new mutant viruses that resist antibod...
Because an immunocompromised host does not produce many antibodies, many viruses must spread. And new mutant viruses that resist antibodies can multiply.
A mutation that allows a virus to evade antibodies is not necessarily advantageous. That could make the virus’ spike protein unstable so it can’t quickly lock onto a cell, for example. But inside a person with a weakened immune system, viruses may be able to acquire a new mutation that stabilizes the spike again.
Similar mutations could have developed over and over again in the same person, Dr Pond speculates, until Omicron developed a breakthrough protein with just the right combination of mutations to allow it to spread extremely well among people. in good health.
“It certainly seems plausible,” said Sarah Otto, an evolutionary biologist at the University of British Columbia who was not involved in the study. But she said scientists still needed to conduct experiments to rule out alternative explanations.
It is possible, for example, that the 13 peak mutations offer no advantage to Omicron. Instead, some of the other peak mutations could make Omicron hit, and the 13 are just for the ride.
“I would be cautious about interpreting the data to indicate that all of these previously deleterious mutations were adaptively favored,” Dr. Otto said.
Dr. Pond also acknowledged that his hypothesis still had major flaws. For example, it is not known why, during a chronic infection, Omicron would have taken advantage of its new “bubble” method of penetrating cells.
“We just lack the imagination,” Dr. Pond said.
James Lloyd-Smith, a disease ecologist at UCLA who was not involved in the study, said the research revealed how difficult it is to piece together the evolution of a virus, even if it appeared recently. “Nature is certainly doing its part to keep us humble,” he said.
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