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
I looked into these lab origin theories for the furin cleavage site last year. The problem with it being a laboratory insertion was that although performing an insertion is relatively easy once you know what to insert, generally it’s beyond current science to independently create mutations for a specific purpose.
It’s a bit beyond me as a non-biologist but my feeling based on the literature was that the lab origin was unlikely. However it is pushed in certain circles partly for ideological reasons, based on evidence that is plausible at first glance but with a lot more digging not entirely convincing evidence.
However, there didn’t really seem to be much neutral expert analysis of the evidence.
> Such furin-mediated activation is unusual in that it occurs in part during virus entry. Our findings may explain the polytropic nature, pathogenicity, and life cycle of this zoonotic coronavirus.
MERS-CoV uses furin cleavage of S1/S2 but it does not bind to ACE2 like SARS-CoV-2.