The Genetics Of Corona Virus

This still remains the most interesting article I've found to date. Granted, my internet search is very, very superficial, but this is a very interesting study, posted back in 2005 by the ncbi.nlm.nih.gov: chloroquine is a potent inhibitor of SARS coronavirus infection and spread.

Two genetic regions on human chromosomes linked with severe Covid-19: The Scientist, June 8,
2020.
variants in two regions—the locus that encodes blood type and a multi-gene cluster on chromosome 3—that were linked to respiratory failure during SARS-CoV-2 infection.

One region the authors identified is the locus that encodes blood type. They found that people with blood type A were at a higher risk for respiratory failure, while blood group O seemed to be protective. 

The odds for those with blood type A to be hospitalized with severe respiratory symptoms were nearly 1.5 times the odds for people with other blood types. 

And those with type O had about two-thirds the odds of being hospitalized as those with other blood types. 

This analysis echoes preprint findings from patient datasets collected in China and New York, which Franke says makes the research team more confident that it’s a real association. 

The other genomic region the researchers identified shows up on the human chromosome 3 and contains several genes of interest. One is SLC6A20, which encodes an amino acid transporter that interacts with ACE2, the main receptor that SARS-CoV-2 uses to get into human cells. Two other genes in this cluster encode immune system–related chemokine receptors: the C-X-C motif chemokine receptor 6 and the CC-motif chemokine receptor 9. Both proteins play a role in T cell differentiation and recruitment during influenza viral infections. 

This region also shows up in publicly available results from the COVID-19 Host Genetics Initiative, which gives it weight, the authors write. 

“From the individual perspective of a patient or those people wandering around with blood group A who may think they’re at higher risk, these effect sizes are going to be very, very small compared to major risk factors such as age and sex,” Fairfax says. The gene cluster on chromosome 3 has an even higher effect size than that of the ABO locus, says Franke, “but we cannot say at the moment which of the many candidate genes is most important. All of them are very attractive in this region.” The odds of being hospitalized with respiratory failure from COVID-19 were 1.77 times higher for those with the variants on chromosome 3 than for people without this genotype.

I'm not sure what "1.5 x the odds" exactly means. Does this mean that for every 150 hospitalized/ICU Covid-19 patients with Type A blood, there were 100 patients with B, O, or AB blood types? I don't know.

From, BMC Medicine, July 15, 2020:

In this study, we investigated genetic susceptibility to COVID-19 by examining DNA polymorphisms in ACE2 and TMPRSS2 (two key host factors of SARS-CoV-2) from ~ 81,000 human genomes. 

We found unique genetic susceptibility across different populations in ACE2 and TMPRSS2. Specifically, ACE2 polymorphisms were found to be associated with cardiovascular and pulmonary conditions by altering the angiotensinogen-ACE2 interactions, such as p.Arg514Gly in the African/African-American population. 

Unique but prevalent polymorphisms (including p.Val160Met (rs12329760), an expression quantitative trait locus (eQTL)) in TMPRSS2, offer potential explanations for differential genetic susceptibility to COVID-19 as well as for risk factors, including those with cancer and the high-risk group of male patients. We further discussed that polymorphisms in ACE2 or TMPRSS2 could guide effective treatments (i.e., hydroxychloroquine and camostat) for COVID-19.