There are two interesting studies that have come out of China and the New England Journal of Medicine. I’ve only skimmed these articles and will need to read them in-depth, but I’m hoping that one of the “real” writers here on Kos will pick this up and add to the topic. Note, there isn’t much there in the first place except one barn-burner of an observation.
To understand the basis of these studies you need to know that we’ve sequenced the entire genome and can go searching through it fairly easily. What researchers have done in these two studies is to take DNA from both kinds of patients, those with mild COVID and those with severe COVID. They then look through their genomes to determine commonalities, What things do those who get a severe form of COVID have in common, and how do those who get a mild form differ, genetically, from those who get the severe form. The New England Journal study was based on GWAS or Genome-Wide Association. The Chinese study was something similar and wasn’t as good as the New England Study (according to my wife, the researcher in blood development). You can find it with the Google,
And, they have an answer. There is a unique region of the genome that susceptible folks have in common.
The two stretches of DNA implicated as harboring risks for severe COVID-19 are known to carry some intriguing genes, including one that determines blood type and others that play various roles in the immune system. In fact, the findings suggest that people with blood type A face a 50 percent greater risk of needing oxygen support or a ventilator should they become infected with the novel coronavirus. In contrast, people with blood type O appear to have about a 50 percent reduced risk of severe COVID-19.
NEJM
If you read that you now understand that a region of genome associated with blood type and with some immune responses is directly associated with a greater risk for severe disease. And that blood type A is significantly at higher risk than blood type O. If you go and read the article you will see that they give data on the research, they looked at lots of folks, and the chromosomal locations of these areas. What they also tell you is that they don’t as of yet know which genes are responsible or how the mechanism works.
Speculatively speaking, blood type is determined by protein expression on blood cells. Long-term I would expect that a subset of specific proteins is being expressed that either increase susceptibility or decrease it. That isn’t much of a statement, but take it to the next step. What if there is a set of proteins expressed that blocks full COVID? This is a hypothesis right out of my little brain. If you repeat it as fact, you are generating a CT. But you can see that if this were true you might be able to generate a therapy by providing those proteins to susceptible patients. That is only one model I can come up with, and I can think of a dozen reasons it might not be viable. But it lets you see how folks might start to think about using this information.
- I want to add an edit. There is a good bit of speculation in the comments about blood type and its impact on this. Those speculations might be correct but this work doesn’t address that. Blood type A is linked to increased severity, but that does not mean it is causative (some sharp commenters below point this out). The most logical route to follow is that there is a gene tightly linked to the A antigen gene that is playing a role, but that isn’t the only possibility.
- Antigen A could be involved. There is some evidence that blood antigens play some roles in immunity and how pathogens gain entry into cells. theconversation.com/…
- It will take some time for the researchers to narrow down the causative agent via more genome analysis, and like those commenting, I anxiously await that result.
- I don’t think it is unfair to be concerned if you are Type A. But like all things COVID, that means being cautious.