Earlier: Pinker’s Wrong: With Coronavirus Going Global, Time For Nationalism...
Well, this is getting really serious: Coronavirus (now increasingly known as COVID-19) has reached Washington, DC [Rector of prominent Washington, D.C., church tests positive for cor..., CBS, March 8, 2020; CPAC chair had brief contact with coronavirus patient at conference..., Fox News, March 8, 2020]. Global panic is in the air: Italy, which appears to be peculiarly vulnerable to COVID-19 as it was to the 1918 Spanish Flu Pandemic ,has reacted with arguably counter-productive ferocity [Leaked coronavirus plan to quarantine 16m sparks chaos in Italy, Guardian, March 8, 2020]. But, although totally repressed by our race-denying Ruling Class—did you know that Kirkland WA, where the bulk of U.S. deaths have occurred, was 11.3% Asian in the 2010 census?—the evidence that there may be an ethnic and/or racial dimension to the disease continues to mount. Which could mean that the Ruling Class is frightening most people too much—and not warning some people enough.
The evidence has been helpfully brought together by Canadian blogger and independent researcher Peter Frost, who has published in such scientific journals as the Journal of Circumpolar Health, on his blog Evo and Proud [Coevolution with the plague, by Peter Frost, Evo and Proud, March 2, 2020].
Frost reports that there have now been three studies which have attempted to test whether or not there might be genetically-based race differences in susceptibility to COVID-19. The first is the one which I discussed last week, [Single-cell RNA expression profiling of ACE2, the putative receptor of Wuhan 2019-nCov, by Yu Zhao et al., bioRxiv, 2020]. As Frost noted in a comment on my piece at the Unz Review:
The authors found that the ACE2 receptor is concentrated in certain cells and that the number of such cells in lung tissue was five times greater in the Asian donor. There was only one Asian donor in the entire sample, and no further description is provided on this “Asian.” However, the chances are low that the same normal distribution would produce such an extreme outlier.
So, we can be cautiously confident that this study provides of evidence for there being race differences in susceptibility to the virus.
A second study, Frost observes, appeared to refute the first. It did not find “significant differences in ACE2 receptor gene expression between Asian and Caucasian lung tissue.” [Bulk and single-cell transcriptomics identify tobacco-use disparity in lung gene expression of ACE2, the receptor of 2019-nCov, by G. Cai, medRxiv, 2020].
However, explains Frost, the problem is that the sample employed from the US and, thus, the term “Asian” may have conflated “East Asian” and “South Asian,” despite these being distinct races. This is a problem I have looked at before.
The third study, which actually has been peer-reviewed and which employed different methods from the first, found that there were large differences between Asians and Non-Asians, and also within the Asian category, with regard to the distribution of the ACE2-receptor [Comparative genetic analysis of the novel coronavirus (2019-nCoV/SARS-CoV-2) receptor ACE2 in different populations, by Y. Cao et al., Cell Discovery, 2020].
Specifically, the authors found that the prevalence of these receptors was greatest among Han Chinese, then “Mixed American” (U.S. population, not broken-up by race) then African, and finally European. The difference between the Chinese and Non-Chinese samples was substantial.
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