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.
In fact, the paper [3] cited in the top comment has the following response to the Wu and Zhao paper you cited:
> The recent acquisition of the FCS by SARS-CoV-2 via a natural insert was proposed by Wu and Zhao (2021) on the basis of the existence of FCS in other, more distant Betacoronaviruses with different loop positions to SARS-CoV-2 and the existence of a partial natural insert in the same region in RmYN02 (Zhou et al. 2020a). The reliability of the conclusions of Zhou et al. (2020a) has been questioned by Deigin and Segreto (2020), who particularly challenge the claim that RmYN02 has an insertion around the site of the FCS insertion in SARS-CoV-2 and instead point to a two amino acid deletion in RmYN02 at that locus. Therefore, RmYN02 should not be used as evidence of the natural origin of SARS-CoV-2′s FCS until its claimed insertion is properly validated.
Disclaimer: I’m no biologist/virologist.
[0] https://www.sciencedirect.com/science/article/pii/S187350612...
[1] https://doi.org/10.1016/j.cub.2020.05.023
[2] https://arxiv.org/abs/2012.00627
[3] https://link.springer.com/article/10.1007/s10311-021-01211-0