In December, Wenfeng Qian, a Beijing-based scientist, and a group of his colleagues, offered a possible answer: mice. In a paper published in the Journal of Genetics and Genomics, they argued that Omicron’s mutations had been subjected to greater pressure to evolve than the other sars-CoV-2 variants, which had evolved in human hosts—indicating, perhaps, that it had evolved in a different species. They also found that some of the mutations in Omicron’s spike are the same mutations that had already been found to help sars-CoV-2 infect mice. (Scientists identified these mutations when they created mouse-adapted strains of sars-CoV-2 in order to research vaccines and therapeutics.) “Collectively, our results suggest that the progenitor of Omicron jumped from humans to mice, rapidly accumulated mutations conducive to infecting that host, then jumped back into humans,” Qian and his co-authors wrote. How infected mice might have infected people is anyone’s guess.

Trevor Bedford, a professor at Fred Hutchinson Cancer Research Center in Seattle, and a leading expert on viral evolution and surveillance, said that Qian’s paper “is the most compelling case for rodent origin I’ve seen.” But Bedford favors a more popular hypothesis—that Omicron evolved in a chronically infected, immunocompromised patient, such as someone who is H.I.V.-positive. “I’d place more likelihood on the chronic infection route,” he wrote in an e-mail, “but definitely not certain of this origin.” Richard Lessells, an infectious-disease physician in South Africa who was part of the team that initially identified Omicron, agreed. “My own view is still that chronic infection and evolution in a human host may be the most likely mechanism.”