Because an immunocompromised host doesnxe2x80x99t produce a lot of antibodies, many viruses are left to propagate. And new mutant viruses that resist the antibodies can multiply.

A mutation that allows a virus to evade antibodies isnxe2x80x99t necessarily advantageous. It could make the virusxe2x80x99s spike protein unstable so that it canxe2x80x99t latch quickly onto a cell, for example. But inside someone with a weak immune system, viruses may be able to gain a new mutation that stabilizes the spike again.

Similar mutations could have built upon themselves again and again in the same person, Dr. Pond speculates, until Omicron evolved a spike protein with just the right combination of mutations to allow it to spread supremely well among healthy people.

xe2x80x9cIt certainly seems plausible,xe2x80x9d 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 run experiments to rule out alternative explanations.

Itxe2x80x99s possible, for example, that the 13 spike mutations offer no benefit to Omicron at all. Instead, some of the other spike mutations could be making Omicron successful, and the 13 are just along for the ride.

xe2x80x9cI would be cautious about interpreting the data to indicate that all of these previously deleterious mutations have been adaptively favored,xe2x80x9d Dr. Otto said.

Dr. Pond also acknowledged that his hypothesis still has some big gaps. For example, itxe2x80x99s not clear why, during a chronic infection, Omicron would have gained an advantage from its new xe2x80x9cbubblexe2x80x9d method for getting into cells.

xe2x80x9cWe just lack imagination,xe2x80x9d Dr. Pond said.

James Lloyd-Smith, a disease ecologist at U.C.L.A. who was not involved in the study, said that the research revealed just how hard it is to reconstruct the evolution of a virus, even one that arose recently. xe2x80x9cNature is certainly doing its part to keep us humble,xe2x80x9d he said.