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Results
"Indel Region 8 includes the S1/S2 junction of the spike protein. Indel 8 of Cambodian bat coronavirus is identical to that of RaTG13 (8 of 8 amino acids) and GD pangolin coronavirus (8 of 8 amino acids), and aside from the lack of the polybasic cleavage site (PRRA) insertion at the S1/S2 junction, it is also homologous to Indel Region 8 of SARS-CoV-2 (8 of 12 amino acids).
The spike proteins of RmYN02 and Thai bat coronavirus viruses share identical or highly similar sequences in every Indel Region (Fig. 1, purple letters, Fig. 2), with 98.0% amino acid identity (99.3% similar amino acids) overall, reflecting their close phylogenetic relationship across the complete genome."
This next section contradicts the thought that the spike protein was engineered as it binds with human lung tissue so well.
"The RaTG13 spike protein shares 97.4% amino acid identity and 98.7% nucleotide sequence similarity with the SARS-CoV-2 spike protein. Although the GD pangolin coronavirus spike has less overall sequence similarity to SARS-CoV-2 spike (89.8% identical, 96.0% similar), it exhibits a larger number of predicted contact residues with ACE2 than RaTG13 (Lam et al., 2020; Andersen et al., 2020). Specifically, the spike protein sequence of the GD pangolin shares 5 of 6 predicted ACE2 contact residues with SARS-CoV-2, compared with only 1of 6 for the RaTG13 spike protein.
The pangolin, the anteater type of animal thought to be the intermediary to humans, its sequence is closer to Covid that the RaTG13 spike protein. Aw heck, I should have read ahead.
Discussion
" The RBD of the Cambodian bat coronavirus provides a divergent example of a sequence that binds ACE2. The binding specificity of Cambodian bat coronavirus RBD remains to be determined. In this regard, there is no evidence that the ACE2 binding solution that SARS-CoV-2 shares in part with Cambodian bat coronavirus as well as RaTG13 and GD pangolin coronavirus is specific for human ACE2. On the contrary, SARS-CoV-2 binds efficiently to ACE2 of several animal species (Wu F et al., 2020; Shang et al., 2020), thereby invalidating claims that the SARS-CoV-2 RBD was either selected or specifically optimized for human ACE2 binding (Zhan, Deverman, and Chan, 2020; Piplai et al., 2020). Further evidence that the SARS-CoV-2 RBD is not specifically adapted to human ACE2 is provided by repeated examples of human-to-animal transfers that require few, if any, RBD mutations (Garry, 2021). Moreover, the RBD is the site of several mutations in newly detected SARS-CoV-2 variants: this suggests that the human ACE2 binding is not optimal and is still subject to adaptive evolution as the virus spreads through the human population (Rambaut et al., 2020; Tegally et al., 2020; Faria et al., 2022). "
The RmYN02 genome was sequenced from a Rhinolophus malayanus sampled in Yunnan province China in June 2019 (Zhou H et al., 2020). The Thai bat coronavirus genome was sequenced from a Rhinolophus acuminatus sampled by an independent research group one year later (Wacharapluesadee al., 2021). The high similarity of the newly-derived spike sequence of Thai bat coronaviruses with RmYN02 spike (98.0% identity, 99.3% similar amino acids over a 1227 amino acid overlap) shows that RmYN02 cannot be a contrived or manipulated virus.
Furin cleavage sites have been noted at the S1/S2 junctions in members of four betacoronavirus subgenuses, and while not universally present, can also be found in other human coronaviruses (Wu and Zhao, 2020). The newly determined S1/S2 junction sequences of Thai, Japanese and Cambodian bat coronaviruses spikes add to evidence that this region of the spike protein represents an evolutionary “hotspot”. Notably, the QTQTNS motif near the S1/S2 cleavage site is present in Cambodian bat coronavirus, RaTG13, GD Pangolin coronavirus and SARS-CoV-2. None of these sequences were determined until after the COVID-19 pandemic began. Likewise, the NSPXX/-AR motif in Thai bat virus, RmYN02 and SARS-CoV-2 spike had not been detected in any coronavirus sequenced prior to 2019. Japan bat coronavirus also has a distinct S1/S2 junction, and provides another example of an apparent insertion near the site. These observations provide further strong evidence for the evolutionary volatility of the S1/S2 cleavage site and that the furin cleavage site arose in SARS-CoV-2 via a natural insertion process (Zhou H et al. 2020).
I have been reading enough lately that I can 'sort' of follow along with this paper as long as I don't get bogged down in the nuts and bolts of it all. While the Chinese may have been doing the type of stuff they think they say and it is conceivable that workers there infected themselves there is no proof that they were hiding the outbreak because they knew they were the source. With the Chinese government, the staff there may have tried to hush it up just to keep their jobs. This last paper found similar viruses in other populations. Basically pours cold water on the manufactured, gain of function theory as the only one rather than it could have came from the wild.
"Indel Region 8 includes the S1/S2 junction of the spike protein. Indel 8 of Cambodian bat coronavirus is identical to that of RaTG13 (8 of 8 amino acids) and GD pangolin coronavirus (8 of 8 amino acids), and aside from the lack of the polybasic cleavage site (PRRA) insertion at the S1/S2 junction, it is also homologous to Indel Region 8 of SARS-CoV-2 (8 of 12 amino acids).
The spike proteins of RmYN02 and Thai bat coronavirus viruses share identical or highly similar sequences in every Indel Region (Fig. 1, purple letters, Fig. 2), with 98.0% amino acid identity (99.3% similar amino acids) overall, reflecting their close phylogenetic relationship across the complete genome."
This next section contradicts the thought that the spike protein was engineered as it binds with human lung tissue so well.
"The RaTG13 spike protein shares 97.4% amino acid identity and 98.7% nucleotide sequence similarity with the SARS-CoV-2 spike protein. Although the GD pangolin coronavirus spike has less overall sequence similarity to SARS-CoV-2 spike (89.8% identical, 96.0% similar), it exhibits a larger number of predicted contact residues with ACE2 than RaTG13 (Lam et al., 2020; Andersen et al., 2020). Specifically, the spike protein sequence of the GD pangolin shares 5 of 6 predicted ACE2 contact residues with SARS-CoV-2, compared with only 1of 6 for the RaTG13 spike protein.
The pangolin, the anteater type of animal thought to be the intermediary to humans, its sequence is closer to Covid that the RaTG13 spike protein. Aw heck, I should have read ahead.
Discussion
" The RBD of the Cambodian bat coronavirus provides a divergent example of a sequence that binds ACE2. The binding specificity of Cambodian bat coronavirus RBD remains to be determined. In this regard, there is no evidence that the ACE2 binding solution that SARS-CoV-2 shares in part with Cambodian bat coronavirus as well as RaTG13 and GD pangolin coronavirus is specific for human ACE2. On the contrary, SARS-CoV-2 binds efficiently to ACE2 of several animal species (Wu F et al., 2020; Shang et al., 2020), thereby invalidating claims that the SARS-CoV-2 RBD was either selected or specifically optimized for human ACE2 binding (Zhan, Deverman, and Chan, 2020; Piplai et al., 2020). Further evidence that the SARS-CoV-2 RBD is not specifically adapted to human ACE2 is provided by repeated examples of human-to-animal transfers that require few, if any, RBD mutations (Garry, 2021). Moreover, the RBD is the site of several mutations in newly detected SARS-CoV-2 variants: this suggests that the human ACE2 binding is not optimal and is still subject to adaptive evolution as the virus spreads through the human population (Rambaut et al., 2020; Tegally et al., 2020; Faria et al., 2022). "
The RmYN02 genome was sequenced from a Rhinolophus malayanus sampled in Yunnan province China in June 2019 (Zhou H et al., 2020). The Thai bat coronavirus genome was sequenced from a Rhinolophus acuminatus sampled by an independent research group one year later (Wacharapluesadee al., 2021). The high similarity of the newly-derived spike sequence of Thai bat coronaviruses with RmYN02 spike (98.0% identity, 99.3% similar amino acids over a 1227 amino acid overlap) shows that RmYN02 cannot be a contrived or manipulated virus.
Furin cleavage sites have been noted at the S1/S2 junctions in members of four betacoronavirus subgenuses, and while not universally present, can also be found in other human coronaviruses (Wu and Zhao, 2020). The newly determined S1/S2 junction sequences of Thai, Japanese and Cambodian bat coronaviruses spikes add to evidence that this region of the spike protein represents an evolutionary “hotspot”. Notably, the QTQTNS motif near the S1/S2 cleavage site is present in Cambodian bat coronavirus, RaTG13, GD Pangolin coronavirus and SARS-CoV-2. None of these sequences were determined until after the COVID-19 pandemic began. Likewise, the NSPXX/-AR motif in Thai bat virus, RmYN02 and SARS-CoV-2 spike had not been detected in any coronavirus sequenced prior to 2019. Japan bat coronavirus also has a distinct S1/S2 junction, and provides another example of an apparent insertion near the site. These observations provide further strong evidence for the evolutionary volatility of the S1/S2 cleavage site and that the furin cleavage site arose in SARS-CoV-2 via a natural insertion process (Zhou H et al. 2020).
I have been reading enough lately that I can 'sort' of follow along with this paper as long as I don't get bogged down in the nuts and bolts of it all. While the Chinese may have been doing the type of stuff they think they say and it is conceivable that workers there infected themselves there is no proof that they were hiding the outbreak because they knew they were the source. With the Chinese government, the staff there may have tried to hush it up just to keep their jobs. This last paper found similar viruses in other populations. Basically pours cold water on the manufactured, gain of function theory as the only one rather than it could have came from the wild.
