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The news that the Omicron strain of SARS-Cov2 has mouse fingerprints all over it probably didn’t rock your world, but it maybe it should. Let’s first explain the mouse part.

Wei et al claim that the molecular spectrum of mutations (i.e., the relative frequency of the 12 types of base substitutions) acquired by the progenitor of Omicron was significantly different from the spectrum for viruses that evolved in human patients but resembled the spectra associated with virus evolution in a mouse cellular environment. In plain language the rates of the different base substitutions (e.g., cytosine to uracil, C→U) are species-dependent and the frequencies the authors found match mice the best. They further claim that mutations in the Omicron spike protein significantly overlap with SARS-CoV-2 mutations known to promote adaptation to mouse hosts, particularly through enhanced spike protein binding affinity for the mouse cell entry receptor. In other words, there’s been a lot of adaptation going on in mice, if this species truly was infected with the omicron progenitor. The theory, that the virus jumped from humans to mice and then back again to humans about a year and half later is only one of several proposed theories. I should also point out that the authors work in China and in a previous paper are definite proponents of the natural origin theory. While not entirely discounting that possibility, the evidence that SARS-Cov2 happened because of a leak from a Chinese bat coronavirus biowarfare program partially funded by the USA is much stronger. If you have any doubt, you should read What Really Happened in Wuhan by Sharri Markson. But, I digress.

Here are the problems with this study and other speculations involving mice. Genetic studies indicate that the omicron strain diverged around May of 2020 and did not reappear until around November of 2021. That’s almost a year-and-a-half where there was no interaction, which is a long time in which nothing happened. Second, it’s not that easy to infect mice with earlier strains of the virus. Based on work done by several research groups it appears that beta and gamma strains can infect mice, and possibly a few alpha strains. These strains surfaced in the late fall of 2020 although it’s possible they might have emerged locally in small numbers of patient a few months earlier. The implication is that it’s a bit of a stretch to suggest that the first zoonotic jump occurred in May 2020. The reverse jump must have occurred in the early fall (say October) of 2021 in order for a human to be infected and that infection to rapidly spread.

So, lots of ifs, which is why many epidemiologists favor another theory that it originated in a human who was immunodeficient. But that theory also suffers from the same problem, namely isolation while the mutations piled up for nearly a year-and-a-half. So, lots of issues with the origin of this strain. I’ll also give you another, perhaps crackpot theory given the dispute over the origin of the initial outbreak in Wuhan: a group of researchers took some mice and infected them successfully around May of 2020, plus or minus a few months. They employed serial gain-of-function testing and perhaps indulged in RNA editing to see what happened over a long period of time. Perhaps one or more of the mice got into the wild.

Regardless of how the omicron strain originated, if there’s any truth to the mouse hypothesis, that means we may have lots of mouse and perhaps rodent populations infected with a SARS-Cov2 strain. Given that rodents are a bit more abundant than bats in the world, I’d say that’s bad news. It means there’s another mammalian repository of the virus to deal with.