>Everyone knows that mutations that increase transmissability generally hurt morbidity. Is there some reason you think this supports zoonotic hypothesis? It is public knowledge RaTG13 was collected from a mine shaft where a similar virus killed 50% of infected workers and where WIV was doing significant sampling work.

Why would this support either hypothesis? The cleavage site clearly has nothing to do with RATG-13 and it is probably one of the main drivers of SARS-CoV-2 pathogenesis. See here:

-https://www.nature.com/articles/s41586-021-03237-4

-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457603/

But before you say "See! Gotcha! That means that the cleavage site is the smoking gun!"

It also looks, from a molecular perspective, like a natural recombination event. See here:

-https://www.frontiersin.org/articles/10.3389/fgene.2020.0078...