The high mutation rate of RNA viruses makes it problematic to understand and resolve the role of recombination in generating genomic variation. Frequent mutations will (1) increase the likelihood of convergent mutations, particularly in regions subject to strong positive selection, causing sequence similarities that can be mistaken for recombination events, and (2) introduce new changes that accumulate and obscure recognition of past recombination events. We analyzed the patterns of recombination across Betacoronaviruses using a dedicated approach to distinguish true recombination from convergent mutations. The Betacoronaviruses comprise several populations that could be considered distinct biological species in that they do not engage in gene flow with one another. Moreover, recombination events within the Sarbecovirus subgenus, which includes SARS-CoV-2, are highly biased and predominate in the spike protein region, implicating recombination as having a substantial role in host tropism and viral ecology
As far as I can tell, this preprint doesn’t invalidate the claim that sarbecoviruses don’t recombine with other more distant clades.
Bottom line: recombination is an unlikely explanation for the origin of the FCS in SARS2.
RaTG13, MP789, and RmYN02 are the strains closest to SARS-CoV-2, and their existence came to light only after the start of the pandemic. Their genomes have been used to support a natural origin of SARS-CoV-2 but after a close examination all of them exhibit several issues. We specifically address the presence in RmYN02 and closely related RacCSxxx strains of a claimed natural PAA/PVA amino acid insertion at the S1/S2 junction of their spike protein at the same position where the PRRA insertion in SARS-CoV-2 has created a polybasic furin cleavage site. We show that RmYN02/RacCSxxx instead of the claimed insertion carry a 6-nucleotide deletion in the region and that the 12-nucleotide insertion in SARS-CoV-2 remains unique among Sarbecoviruses. Also, our analysis of RaTG13 and RmYN02’s metagenomic datasets found unexpected reads which could indicate possible contamination. Because of their importance to inferring SARS-CoV-2′s origin, we call for a careful reevaluation of RaTG13, MP789 and RmYN02 sequencing records and assembly methods.
That does not substantiate the claim I asked for substantiation of.
You wrote:
What this means is that the viruses that are phylogenetically closest to SARS2, i.e. those that can recombine with each other, do not have an FCS.
“Those that can recombine with each other” implies viruses other than those “phylogenetically closest to SARS2” can’t recombine with SARS2. The article you reference instead says that recombination between different betacoronavirus subgenera does not appear to have contributed measurably to their evolution.
Nothing in that paper substantiates this claim. At best it would argue that, statistically speaking, such a recombination event is unlikely to be from a betacoronavirus outside of the sarbecovirus clade. On the contrary the article says recombination in the spike protein, within that clade, is rather rampant.
I don’t really understand that paper very well, as it is quite technical. Can you provide a plain English summary of it, and why you believe it supports the claim that the virus was artificially created?
I’d also be interested in hearing why you are now accepting the sort of genetic research that you deny when it demonstrates common ancestry to be true, but that’s probably a topic for another discussion…
That’s correct. But since no known sarbecovirus except SARS2 has a FCS, it follows that recombination is an unlikely explanation for origin of the FCS in SARS2.
I saw a comment on a YouTube conversation thread that read,
“the wrong guy” was RIGHT.
Certainly, it is nearly impossible to say that there is not an element of this being true. Sad. It indicates partisanship that overrides truth-seeking.
First, you ignore the fact that furin CS’s have independently in different lineages of the betacoronaviruses. That we find one in a lineage of one of the Sarbecoviruses (subgenera of the Betacoronaviruses) is just unremarkable.
Second, you seemed to suggest that only those clade members “phylogenetically closest” to SARS-CoV-2 could have recombined with it to produce its FCS and since none of its closest relatives have a furin CS, therefore its presence in SARS-CoV-2 seems suspicious. You then went on to cite a paper that you think supports your contention that SARS-COV-2 hasn’t recombined with distantly related betacoronaviruses. However, the paper you cited betrays your position. The study used the “h/m” ratio to detect recombination: higher h/m ratios suggest marked recombination, while lower h/m ratios suggests little or no recombination. Now see this excerpt:
The researchers went further to test if these homoplasies were due to recombination or convergent evolution and not surprisingly some of them were due to recombination as shown below. :
So we see recombination between SARS-CoV-2 and some bat merbecoviruses (which are quite distant relatives), refuting your position that only strains closest to SARS-CoV-2 recombined with it. In addition, among the Sarbecovirus genomes there is extensive recombination, especially in the spike protein region. Check Fig 2 yourself and see what the paper says:
What the authors found was no evidence for recombination among SARS-CoV-2 genomes, not between SARS-CoV-2 and other betacoronaviruses.
You misunderstood the paper and I hope its now obvious how.
We got a bit derailed into definition of “conspiracy theory” and whether and where it should be used, etc. and a bit on the political side of SARS-CoV-2 origins. I split that discussion off into a Side Conversation. As long as that conversation stays civil it is welcome to continue, but we should keep this conversation more focused on evidence and the science in determining the origins of a virus.
BrianLopez