Great stream with Doc and Crawford ! Thank you for all your work and sacrifice. Thank you for fighting for those that are victims, and those that can no longer speak.
In the paper by Ali et al. from 2020 where they looked at the frequency of six ACE2 alleles, the K26R allele was the only allele which was modeled as beneficial, and it was shown to have the highest frequency in Ashkenazis. However the paper only included six other populations besides Ashkenazis, and most of the samples in the paper were from gnomAD. In gnomAD v3, the frequency of the K26R allele is only about 1.3% in Ashkenazis, so it won't make much difference if it only gives an advantage to about 1% of Ashkenazis. And on gnomAD v3, the frequency of the K26R allele is about 0.7% in non-Ashkenazi-non-Finnish Europeans, so the frequency in Ashkenazis is only about 0.6 percentage points higher.
When I took the modeled binding energy of each ACE2 allele from the paper by Ali et al., and I calculated a weighted average of the binding energies multiplied by the frequency of each allele at gnomAD v3, the total binding energy was about -40.175 kcal/mol for Ashkenazis and about -40.207 kcal/mol for non-Ashkenazi non-Finnish Europeans, so there was virtually no difference.
And another problem with the K26R theory is that there's two papers where the K26R allele was modeled as detrimental and not beneficial. The other paper said: "Three SNVs, E329G (rs143936283), M82I (rs267606406) and K26R (rs4646116), had a significant reduction in binding free energy, which indicated higher binding affinity than wild-type ACE2 and greater susceptibility to SARS-CoV-2 infection for people with them." And the other paper said: "The K26, which is just proximal to the first region of the ACE2 receptor involved in S-protein binding, has been shown previously to bind the sterically hindering first mannose in the glycan that is linked to N90 and thus stabilizes the glycan moiety hindering the binding of S-protein RBD to ACE2 [41] (Figure 2A). The missense variant R26 creates a new hydrogen bond with D30, which is then poised to build a salt-bridge with the S-protein RBD K417 that increases the affinity of SARS-CoV-2 to the ACE2 receptor [21] (Figure 2B). Indeed, the ACE2 K26R activating variant was extremely rare in East Asian (MAF = 0.007%), Africans (MAF = 0.095%), but the second most common variant in Europeans with MAF of 0.587% (shown in green fonts in Table 1). The MAF of this variant in the Kuwaiti population was nearly half that of Europeans (MAF = 0.29%), and it was absent from the Qatari and Iranian exome data (Table 1). Our structural modeling supports the notion that K26R is an ACE2 receptor activating variant (Figure 2A, B). Consistent with these findings, using a synthetic human ACE2 mutant library, a recent study reported that the R26 variant increased S-protein binding and susceptibility to the virus significantly [42]."
When RFK got in trouble for his comments about race-specific bioweapons, he linked to another paper which he said showed that "COVID-19 appears to disproportionately affect certain races since the furin cleave docking site and least compatible with ethnic Chinese, Finns, and Ashkenazi Jews". However the paper RFK linked looked at populations from gnomAD v3, so it only included 8 other populations besides Ashkenazis, and other populations missing from gnomAD may have had a more advantageous mutation profile than Ashkenazis. In the main text of that paper, there were only two references to Ashkenazis, which were in a figure which showed that Ashkenazi and Amish samples had zero occurrences of ACE2 alleles which were modeled as detrimental, and in another part of the paper which referred to the same figure. However Ashkenazis and Amishes have a small population size at gnomAD v3, and populations with a small sample size are less likely to have one or more occurrences of a rare deleterious allele than populations with a large sample size. So for example at gnomAD v3, total number of samples that have been typed for the K26R allele is 53,215 for non-Finnish-non-Ashkenazi Europeans but only 2,650 for Ashkenazis and 684 for Amishes.
Finished watching. The last hour was absolutely riveting. I don’t know enough yet to understand all this very well, but I have no doubt that it’s super important.
The link has problems as of this moment. Spaces in the link?
http://biowarfare%20hypothesis%20examined%20-%20rounding%20the%20earth%20round%20table%20w/%20with%20Dr%20Kevin%20McCairn,%20Charles%20Rixey
Very much looking forward to the stream!
It is all nanotech toxicity poisoning, not a virus. Nanotechnology/graphene has specific mechanisms of toxicity, observed in this so-called "Covid"
https://outraged.substack.com/p/the-government-and-all-political
Great stream with Doc and Crawford ! Thank you for all your work and sacrifice. Thank you for fighting for those that are victims, and those that can no longer speak.
Glad to see you posting again, Charles. Happy Thanksgiving!
Even the smallest bit of information from you is valued my friend, God Bless you Mr. Charles Rixey
Mathew Crawford is a pain the neck. What a pity he was part of the conversation.
I have shown McCairn many times why the K26R allele is not significant: https://mongol-fi.github.io/rfkracespecific.html.
In the paper by Ali et al. from 2020 where they looked at the frequency of six ACE2 alleles, the K26R allele was the only allele which was modeled as beneficial, and it was shown to have the highest frequency in Ashkenazis. However the paper only included six other populations besides Ashkenazis, and most of the samples in the paper were from gnomAD. In gnomAD v3, the frequency of the K26R allele is only about 1.3% in Ashkenazis, so it won't make much difference if it only gives an advantage to about 1% of Ashkenazis. And on gnomAD v3, the frequency of the K26R allele is about 0.7% in non-Ashkenazi-non-Finnish Europeans, so the frequency in Ashkenazis is only about 0.6 percentage points higher.
When I took the modeled binding energy of each ACE2 allele from the paper by Ali et al., and I calculated a weighted average of the binding energies multiplied by the frequency of each allele at gnomAD v3, the total binding energy was about -40.175 kcal/mol for Ashkenazis and about -40.207 kcal/mol for non-Ashkenazi non-Finnish Europeans, so there was virtually no difference.
And another problem with the K26R theory is that there's two papers where the K26R allele was modeled as detrimental and not beneficial. The other paper said: "Three SNVs, E329G (rs143936283), M82I (rs267606406) and K26R (rs4646116), had a significant reduction in binding free energy, which indicated higher binding affinity than wild-type ACE2 and greater susceptibility to SARS-CoV-2 infection for people with them." And the other paper said: "The K26, which is just proximal to the first region of the ACE2 receptor involved in S-protein binding, has been shown previously to bind the sterically hindering first mannose in the glycan that is linked to N90 and thus stabilizes the glycan moiety hindering the binding of S-protein RBD to ACE2 [41] (Figure 2A). The missense variant R26 creates a new hydrogen bond with D30, which is then poised to build a salt-bridge with the S-protein RBD K417 that increases the affinity of SARS-CoV-2 to the ACE2 receptor [21] (Figure 2B). Indeed, the ACE2 K26R activating variant was extremely rare in East Asian (MAF = 0.007%), Africans (MAF = 0.095%), but the second most common variant in Europeans with MAF of 0.587% (shown in green fonts in Table 1). The MAF of this variant in the Kuwaiti population was nearly half that of Europeans (MAF = 0.29%), and it was absent from the Qatari and Iranian exome data (Table 1). Our structural modeling supports the notion that K26R is an ACE2 receptor activating variant (Figure 2A, B). Consistent with these findings, using a synthetic human ACE2 mutant library, a recent study reported that the R26 variant increased S-protein binding and susceptibility to the virus significantly [42]."
When RFK got in trouble for his comments about race-specific bioweapons, he linked to another paper which he said showed that "COVID-19 appears to disproportionately affect certain races since the furin cleave docking site and least compatible with ethnic Chinese, Finns, and Ashkenazi Jews". However the paper RFK linked looked at populations from gnomAD v3, so it only included 8 other populations besides Ashkenazis, and other populations missing from gnomAD may have had a more advantageous mutation profile than Ashkenazis. In the main text of that paper, there were only two references to Ashkenazis, which were in a figure which showed that Ashkenazi and Amish samples had zero occurrences of ACE2 alleles which were modeled as detrimental, and in another part of the paper which referred to the same figure. However Ashkenazis and Amishes have a small population size at gnomAD v3, and populations with a small sample size are less likely to have one or more occurrences of a rare deleterious allele than populations with a large sample size. So for example at gnomAD v3, total number of samples that have been typed for the K26R allele is 53,215 for non-Finnish-non-Ashkenazi Europeans but only 2,650 for Ashkenazis and 684 for Amishes.
Listened. Pity you were interrupted so much you could hardly complete a sentence.
Thanks for posting. I'm still only half way through watching it, but so far it has been fascinating (although all over the place).
Finished watching. The last hour was absolutely riveting. I don’t know enough yet to understand all this very well, but I have no doubt that it’s super important.