Because an immunocompromised host does not make many antibodies, many viruses continue to reproduce. And new mutant viruses that resist the antibodies can multiply.
A mutation that allows a virus to evade antibodies is not necessarily beneficial. It can make the virus’s spike protein unstable, so that it can’t quickly attach to a cell, for example. But within someone with a weak immune system, viruses could potentially acquire a new mutation that stabilizes the spike again.
Similar mutations could build on their own in the same person over and over, speculates Dr. Pound, until Omicron developed a spike protein with just the right combination of mutations to allow it to spread superbly among healthy people.
“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 had to conduct experiments to rule out alternative explanations.
For example, the 13 spike mutations may not provide Omicron with any benefit at all. Instead, some of the other spike mutations could make Omicron successful, and the 13 are just along for the ride.
“I would be careful interpreting the data to indicate that all of these previously deleterious mutations are adaptively favored,” said Dr. Otto.
dr. Pond also acknowledged that his hypothesis still has major gaps. For example, it’s not clear why Omicron would have benefited from its new “bubble” method of getting into cells during a chronic infection.
“We just lack imagination,” said Dr. Lb.
James Lloyd-Smith, a disease ecologist at UCLA who was not involved in the study, said the study revealed how difficult it is to reconstruct the evolution of a virus, even one that emerged recently. “Nature certainly does its part to keep us humble,” he said.
