I wasn't familiar with that theory, so leaning on others here (I'm taking out the cites since it really muddles the readability but they're in the source file).

I wasn't familiar with that theory, so leaning on others here (I'm taking out the cites since it really muddles the readability but they're in the source file). This all makes sense to me; > A specific laboratory escape scenario involves accidental infection in the course of serial passage of a SARSr-CoV in common laboratory animals such as mice. However, early SARSCoV-2 isolates were unable to infect wild-type mice. Although murine models are useful for studying infection in vivo and testing vaccines, they often result in mild or atypical disease in hACE2 transgenic mice. These findings are inconsistent with a virus selected for increased pathogenicity and transmissibility through serial passage through susceptible rodents. Although SARS-CoV-2 has since been engineered and mouse-adapted by serial passage, specific mutations in the spike protein, including N501Y, are necessary for such adaptation in mice. Notably, N501Y has arisen convergently in multiple SARS-CoV-2 variants of concern in the human population, presumably being selected to increase ACE2 binding affinity. > If SARS-CoV-2 resulted from attempts to adapt a SARSr-CoV for study in animal models, it would likely have acquired mutations like N501Y for efficient replication in that model, yet there is no evidence to suggest such mutations existed early in the pandemic. Both the low pathogenicity in commonly used laboratory animals and the absence of genomic markers associated with rodent adaptation indicate that SARS-CoV-2 is highly unlikely to have been acquired by laboratory workers in the course of viral pathogenesis or gain-of function experiments. Basically if you wanted to study sars cov2 in transgenic mice with adapted hACE2 receptors, there are obvious mutations that you would engineer into the virus to make it more stable and pathogenic. None of these mutations existed in the first samples. But importantly, when covid was spreading in humans, these same mutations naturally appeared through convergent evolution in several variants. Contrary to many claims, the virus wasn't close to being optimized for pathogenicity which would've been the ostensible purpose of GoF research. It really "acts" like it was recently passed to an intermediate host, then fairly quickly began to infect humans. [https://www.cell.com/cell/pdf/S0092-8674(21)00991-0.pdf https://www.cell.com/cell/pdf/S0092-8674(21)00991-0.pdf]