More than a year after the initial documented cases in Wuhan, the source of SARS-CoV-2 has yet to be identified, and the search for a direct or intermediate host in nature has been so far unsuccessful.
The low binding affinity of SARS-CoV-2 to bat ACE2 studied to date does not support Chiroptera as a direct zoonotic agent. Furthermore, the reliance on pangolin coronavirus receptor binding domain (RBD) similarity to SARS-CoV-2 as evidence for natural zoonotic spillover is flawed, as pangolins are unlikely to play a role in SARS-CoV-2′s origin and recombination is not supported by recent analysis.
At the same time, genomic analyses pointed out that SARS-CoV-2 exhibits multiple peculiar characteristics not found in other Sarbecoviruses.
A novel multibasic furin cleavage site (FCS) confers numerous pathogenetically advantageous capabilities, the existence of which is difficult to explain though natural evolution...
source: https://link.springer.com/article/10.1007/s10311-021-01211-0
> https://www.sciencedirect.com/science/article/pii/S187350612...
They exist in the human HCoV-HKU1, HCoV-OC43, MERS-CoV and appear to have evolved independently at least 6 times in betacoronaviruses.
Furthermore while this article claims that the furin cleavage site has not found in any sarbecoviruses, that is now outdated information:
> "Evidence for SARS-CoV-2 related coronaviruses circulating in bats and pangolins in Southeast Asia"
> https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7873279/
Both RacCS203 (91.5% similar to SARS-CoV-2) and RmYN02 (93.3% similar to SARS-CoV-2) have furin cleavage sites. So we're up to 7-to-9 times now that evolution has evolved a furin cleavage site in betacoronaviruses, including 3 sarbecoviruses that may or may not be directly related.
The whole "furin cleavage site is an indication of human engineering" argument is just falsified at this point.