Transmission via intermediary species is obviously possible. That the virus has 96% genetic structure to a known RatGN-13 virus in horseshoe bat i s not disputed. Neither is the real possiblity of SARS-Cov-2 originating in a natural gene swapping. What is not credible are the naive assertions of experts discounting a possible lab origin, by repeating essentially the “straw man” argument by K.G.Andersen, asserting that “synthetic lab origin” is impossible because of its proximity to known bat viruses. But no-one is arguing that. There is a very real possibility that a bat virus was modified in WCDC lab by inserting new genetic sequences and the resulting product escaping. This scenario appears even more real when one learns that the head of the bat viruses research in Wuhan, She Zhengli, conducted virus recombination in the lab for a number of years, and published papers on it.
But there is little evidence of recent major recombination in the history of this particular virus, since its common ancestor with the 2013 virus. It looks like it has a pretty much vertical inheritance from its common ancestor with the 2013 bat sequence.
Check out the paper “Evolutionary origins of the SARS‐CoV‐2 sarbecovirus lineage responsible for the COVID-19 pandemic” (https://www.biorxiv.org/content/10.1101/2020.03.30.015008v1). They run a sliding window along the SARS-CoV-2 sequence and compare it to the sequence of many other viruses. The conservation is not constant across the genome, but different regions are under different evolutionary constraint, and the *relative* conservation across the genome looks more or less consistent rather than there being big sharp jumps in homology as you would expect from distant recombination and see in other more distantly related viruses.
Some have argued that recombination could account for the origin of the specific receptor binding domain since it seems very similar to that found in a pangolin virus. But overall there is very little recombination evidence.
The only idea that is really open at all is ‘Poor procedure resulting in viral transfer from a wild lab animal’, not ‘recombination experiments in the lab creating something unusual’.
Transmission via intermediary species is obviously possible. That the virus has 96% genetic structure to a known RatGN-13 virus in horseshoe bat i s not disputed. Neither is the real possiblity of SARS-Cov-2 originating in a natural gene swapping. What is not credible are the naive assertions of experts discounting a possible lab origin, by repeating essentially the “straw man” argument by K.G.Andersen, asserting that “synthetic lab origin” is impossible because of its proximity to known bat viruses. But no-one is arguing that. There is a very real possibility that a bat virus was modified in WCDC lab by inserting new genetic sequences and the resulting product escaping. This scenario appears even more real when one learns that the head of the bat viruses research in Wuhan, She Zhengli, conducted virus recombination in the lab for a number of years, and published papers on it.
But there is little evidence of recent major recombination in the history of this particular virus, since its common ancestor with the 2013 virus. It looks like it has a pretty much vertical inheritance from its common ancestor with the 2013 bat sequence.
Check out the paper “Evolutionary origins of the SARS‐CoV‐2 sarbecovirus lineage responsible for the COVID-19 pandemic” (https://www.biorxiv.org/content/10.1101/2020.03.30.015008v1). They run a sliding window along the SARS-CoV-2 sequence and compare it to the sequence of many other viruses. The conservation is not constant across the genome, but different regions are under different evolutionary constraint, and the *relative* conservation across the genome looks more or less consistent rather than there being big sharp jumps in homology as you would expect from distant recombination and see in other more distantly related viruses.
Some have argued that recombination could account for the origin of the specific receptor binding domain since it seems very similar to that found in a pangolin virus. But overall there is very little recombination evidence.
The only idea that is really open at all is ‘Poor procedure resulting in viral transfer from a wild lab animal’, not ‘recombination experiments in the lab creating something unusual’.