To a great extent much of the population genetics of humans in the 20th-century that doesn’t involve external traits is the population genetics of blood groups. A, B, and O, along with Rhesus factor. Read L. L. Cavalli-Sforza and William Bodmer’s The Genetics of Human Populations, the first edition of which was written in the 1960s. The emergence of more genetic markers, and Y, mtDNA, and genome-wide analysis has marginalized the exploration of population genetic variation of ABO. But it’s still useful. And it’s still functionally important (there’s a reason that A and B groups evolved!).
Many years ago while reading Alan Templeton’s Population Genetics and Microevolutionary Theory I stumbled upon the fact that spontaneous abortion (miscarriage) is associated with blood group differences between mother and fetus on 
the ABO blood groups. Basically, women who are O (and so genotype OO) have issues with fetuses that express A or B antigen. This isn’t deterministic, just a change in probabilities (I’m A, my wife is O, and our children are a mix, as my genotype is AO).
ABO has also been associated with different risks to different diseases (e.g., it is well known that those who express blood group B are more at risk for Hepatitis B).
So with that, a new preprint, ABO blood group and susceptibility to severe acute respiratory syndrome:
…The ABO group in 3694 normal people in Wuhan showed a distribution of 32.16%, 24.90%, 9.10% and 33.84% for A, B, AB and O, respectively, versus the distribution of 37.75%, 26.42%, 10.03% and 25.80% for A, B, AB and O, respectively, in 1775 COVID-19 patients from Wuhan Jinyintan Hospital. The proportion of blood group A and O in COVID-19 patients were significantly higher and lower, respectively, than that in normal people (both P < 0.001). Similar ABO distribution pattern was observed in 398 patients from another two hospitals in Wuhan and Shenzhen. Meta-analyses on the pooled data showed that blood group A had a significantly higher risk for COVID-19 (odds ratio-OR, 1.20; 95% confidence interval-CI 1.02~1.43, P = 0.02) compared with non-A blood groups, whereas blood group O had a significantly lower risk for the infectious disease (OR, 0.67; 95% CI 0.60~0.75, P < 0.001) compared with non-O blood groups. In addition, the influence of age and gender on the ABO blood group distribution in patients with COVID-19 from two Wuhan hospitals (1,888 patients) were analyzed and found that age and gender do not have much effect on the distribution…
It looks like from their data that A individuals were:
1) more likely to get infected
2) more likely to have severe responses
The individual difference is modest. You aren’t invulnerable if you are O. But, this might impact the course and severity of COVID-19 as it runs through populations…
Here is the table:
South China Morning Post has a good write-up. Here are blood group distributions if you don’t know them offhand (they are pre-Columbian):
(I’m A, my wife is O, and our children are a mix, as my genotype is AO).
My family and I are exactly the same.
By the way, my wife decided to cancel all elective procedures at her facility and the corporate overlords and the board agreed. All the other facilities in the area have done it already or are following suit.
At my own board meeting (via internet), I cast my aye vote to the proposal from the management team to shut everything down and devote all resources to combating the virus. There are related plans to keep other essential services (e.g. labor and delivery) operating with freed up resources and personnel. No nay vote.
I notice the 95% confidence intervals for the A group cases overlap with the control (I hope my calcs are correct!):
Control A: 1188/3694 = 32.16 +- 2.7 (=29.46-34.86)
Jinyintan A: 670/1775 = 37.75 +- 3.7 (=34.05-41.45)
(The B and AB do as well, but the 95% ranges for the O group are distinct: 31.14-36.54 for control vs 21.7-29.9 for the hospital.)
I’m by no means an expert in this, but might this suggest the A result could be due to natural variation in the sampling? … I don’t know how the OR/p-values are calculated so it’s possible they account for this already.
yeah. focus on the O, not the A. otoh, https://academic.oup.com/glycob/article/18/12/1085/1988773 (mechanistic evidence for SARS-cov being better able to get at “A”)
>O master race. I am O
I may indulge my impulse after all, to boldly march directly through the quarantined zones to leer at their ghostly masked existence
Sorry about being off-topic, but why is group O so much more prevalent in the New World?
1) drift
2) more likely O is ancestral, A and later B mutated
As far as I remember every blood group has a different strength and weakness (smallpox, plague, leprosy etc.).
So the distribution of the blood groups today in the Old World might be to a large degree the result of past pandemics and endemic disease herds plus drift and migration. Selection definitely played a role.
Even if the effect was much smaller than with sickle cells and Malaria, considering how many people died e.g. of smallpox even a slight advantage would pay off.
I wonder if Rhesus factor has anything to do with risk of infection?
They don’t mention it in the paper. The vast majority (if not nearly all) of Han are rhesus positive.
Meh.
Sure, blood types are part of the immune system, so this is a mechanistic hypothesis. But everything is correlated with everything. These two samples are different, but there are lots of ways that could happen. Where did this control group come from? Is it really representative of the city? Maybe the outbreak spread through some social network that just happened to be different. For example, I bet that the Korean megachurch didn’t have representative blood types.