Couldn't be bothered going over the whole thing in my state, so will look at a bit and assume the rest is just as bad.
The furin cleavage site. The furin cleavage site is a minute part of the virus’s anatomy but one that exerts great influence on its infectivity. It sits in the middle of the SARS2 spike protein. It also lies at the heart of the puzzle of where the virus came from.
Viruses have all kinds of clever tricks, so why does the furin cleavage site stand out? Because of all known SARS-related beta-coronaviruses, only SARS2 possesses a furin cleavage site. All the other viruses have their S2 unit cleaved at a different site and by a different mechanism.
Furin cleavage sites are common in beta-coronaviruses. Thye look to have evolved independently multiple times:
https://www.sciencedirect.com/science/a ... 6120304165
Seems like a fairly major thing to omit. Even MERS has a furin site.
Recombination is an inadvertent swapping of genomic material that occurs when two viruses happen to invade the same cell, and their progeny are assembled with bits and pieces of RNA belonging to the other. Beta-coronaviruses will only combine with other beta-coronaviruses but can acquire, by recombination, almost any genetic element present in the collective genomic pool. What they cannot acquire is an element the pool does not possess. And no known SARS-related beta-coronavirus, the class to which SARS2 belongs, possesses a furin cleavage site.
This makes no sense. SARS causing beta-coronaviruses can only recombine with other SARS causing beta-coronaviruses? That's just flat out wrong. Beta-coronaviruses, whether they cause SARS or not, can happily recombine.
https://virological.org/t/naturally-occ ... spikes/560
Previously one of us (WRG) presented additional strong evidence that the furin cleavage site insertion in SARS-CoV2 was generated via a natural process (Gallaher, 2020c). Although the 12 base insertion preserves the reading frame, the insertion is out-of-frame. It is highly implausible that any scientist attempting to insert a furin cleavage site would do so by making an out-of-frame insertion. Previous studies that introduced furin cleavage sites in SARS-CoV and MERS-CoV spike genes did not introduce insertions (Follis et al., 2006; Yang et al., 2015). Nor is it likely that any laboratorian would have engineered a change in the SARS-CoV-2 spike that purposefully resulted in prediction of O-linked glycan sites.
https://virological.org/t/tackling-rumo ... ov2019/384
RaTG13, or anything nearly identical to it at the RNA level, simply could not be a proximal source of nCoV2019. It just LOOKS like it might be…at first glance.
Given that furin cleavage signals are present in other coronaviruses at exactly that point in the S1/S2 boundary region, it only LOOKS unusual, especially against the backdrop of SARS. The preponderance of evidence, coupled with Ockham’s razor (that the simplest explanation is preferred) dictates that the PRRA sequence has been conserved in nCoV2019 from a long ago ancestor virus. It is not of suspicious origin. The closest bat virus sequence is really not close at all.
This also from Bill Gallaher is interesting:
In HKU9 they code for TSAG in the loop region known in the Gao terminology as SD3. The first CT of the putative insert is still orphan, but there is a relevant possible source for the rest, albeit out of frame.
The “Insert” is CT CCTCGGCGGG, the last ten identical to the sequence in HKU9.
The sequence context has other similarities, i.e the “cagac” upstream and a “c” downstream of the “insert” as aligned here:
HKU9 gcatttgta caga------cctcggcgggc ctctgt
CoV-2 tatcagact cagac ttgct cctcggcgggc acgtagt
Total of 14 of 19 identical nucleotides in two runs with one gap. That’s a lock.
Copy choice errors in mixed infections do not have to be in an exact context, since it is not a recombination, but RNA polymerase hopping from one template strand to another. In this case the two templates code for the same gene, between regions about a thousand nucleotides from one another, out of a genome of 30,000 nucleotides. There could easily have been evolution of the site since the mixed infection, over a period of years.
CHecked this using BLAST, and it's correct:
Query 1 CAGACCTCGGCGGGC 15
Sbjct 24190 CAGACCTCGGCGGGC 24204
Shows how the less common codon usage in the furin site quite possibly came to be in SARS-COV2.
Given all this is relatively well known and completely ignored in the OP's article, I'm going to conclude he has an agenda and is only presenting info that supports his case - not really the done thing in science (but fine on PR).