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Henrietta Lacks was a G6PD Deficiency Type A carrier (her son was hemizygous and hospitalized for it.) Evidently, the HeLa cell line inherited her pathogenic variant as a remarkable feature:
There have been speculations that G6PD deficiency might account for the unusually high mortality rate in Algiers, Spain and Italy... but there are other countries, Greece for example, with high rates of G6PD deficiency of other genotypes/phenotypes where the populations are not experiencing higher morbidity per case, ARDS, etc.
It is possible that Type A adds some specific mechanism missing in other phenotypes.
Researchers may just be observing a coincidence of population genetics. ACE2 and G6PD are on the X chromosome. It would be likely that any two X-linked variants in Ms. Lacks' ancestry would tend to be distributed in the same populations.
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I have been watching and waiting for evidence to emerge with detail on how well-adapted SARS-CoV-2 might be to infecting HeLa cells. There have been numerous reports on increased risk (and decreased risk) alleles on ACE2.
The HeLa genome is restricted, but if anyone has access and can compare HeLA ACE2 to known risk alleles, that could be interesting.
I have read all of the papers referenced here from the Wuhan researchers and they appear to have always used HeLa cell lines, where applicable.
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Adaptation to HeLa may provide the model that explains why such strikingly disproportionate numbers of the U.S.' severe youth cases, and the U.S.' COVID-19 deaths in general, are African American. The youth morbidity rate disparity is extreme in some U.S. areas, like >=75%. If you summed the disparities in underlying conditions I expect it would not account for these numbers.
Please do not take this speculation as a casual dismissal of the disadvantages and systemic problems in the U.S. that affect Black Americans and surely contribute to worsening COVID-19 outcomes. I am speculating that there is an additional factor in the genetics that specifically targets people genetically near to Henrietta Lacks, which would be an artifact of a "Lab Escape" scenario.
The text was updated successfully, but these errors were encountered:
...And/or to take advantage of other specific features of a HeLa cell, like G6PD deficiency:
Does G6PD Deficiency Relate to COVID-19 Infection? - MedPage Today
Henrietta Lacks was a G6PD Deficiency Type A carrier (her son was hemizygous and hospitalized for it.) Evidently, the HeLa cell line inherited her pathogenic variant as a remarkable feature:
Old 1976 Science Mag - Genetic Characteristics of the HeLa Cell - https://www.jstor.org/stable/1741942?seq=1
Archives of Pathology - Henrietta Lacks, HeLa Cells, and Cell
Culture Contamination
There have been speculations that G6PD deficiency might account for the unusually high mortality rate in Algiers, Spain and Italy... but there are other countries, Greece for example, with high rates of G6PD deficiency of other genotypes/phenotypes where the populations are not experiencing higher morbidity per case, ARDS, etc.
It is possible that Type A adds some specific mechanism missing in other phenotypes.
Researchers may just be observing a coincidence of population genetics. ACE2 and G6PD are on the X chromosome. It would be likely that any two X-linked variants in Ms. Lacks' ancestry would tend to be distributed in the same populations.
--
I have been watching and waiting for evidence to emerge with detail on how well-adapted SARS-CoV-2 might be to infecting HeLa cells. There have been numerous reports on increased risk (and decreased risk) alleles on ACE2.
The HeLa genome is restricted, but if anyone has access and can compare HeLA ACE2 to known risk alleles, that could be interesting.
I have read all of the papers referenced here from the Wuhan researchers and they appear to have always used HeLa cell lines, where applicable.
--
Adaptation to HeLa may provide the model that explains why such strikingly disproportionate numbers of the U.S.' severe youth cases, and the U.S.' COVID-19 deaths in general, are African American. The youth morbidity rate disparity is extreme in some U.S. areas, like >=75%. If you summed the disparities in underlying conditions I expect it would not account for these numbers.
Please do not take this speculation as a casual dismissal of the disadvantages and systemic problems in the U.S. that affect Black Americans and surely contribute to worsening COVID-19 outcomes. I am speculating that there is an additional factor in the genetics that specifically targets people genetically near to Henrietta Lacks, which would be an artifact of a "Lab Escape" scenario.
The text was updated successfully, but these errors were encountered: