Important to note that the author suggests that the best fit from observed blood type disease risk differences to a model like this would indicate that getting a virus from someone with an incompatible blood type would be about 40% as easy as getting infected from a compatible blood type.
One might be able to make arguments about intra-familial transmission versus extra-familial transmission rates with more math than I have time for right now.
In this model, if you ignore secretion status, type O people would be hardest to infect but most likely to spread. In the US about 45% of the population is type O, about 40% is type A, about 11% is type B, and about 4% is type AB according to the first source I found. You get the following fractions of the population being easy to transmit to and receive from for each blood type:
O—to 100%, from 45%
B—to 15%, from 56%
A—to 44%, from 85%
AB—to 4%, from 100%
If you assume that you are 40% as likely to spread to someone of a noncompatible blood type, you get a ease-of-infecting-others score for each type of: O = 100%, B = 49%, A = 66%, AB = 42%. Assuming you don’t know their secretion/nonsecretion status.
If you take into account non-secretors, then this is all slightly wrong and you actually have most non-O people slightly less infectious than that and some people who are A, B, or AB with their usual higher risk of getting infected but who transmit like type O. This is me—I am a type A nonsecretor and thus would be more vulnerable to transmission from a full 85% of the population, while being good at transmitting to 100% of the population. Such individuals might be more likely to be important nodes in the network.
If you look at the paper they show that the biggest result of this kind of an effect on an epidemiological model is that the more diverse the population is in terms of blood types—a more even distribution of A, B, and O—the slower spread happens, and the more homogenous a population is in terms of blood type the faster it happens regardless of which blood type is dominant.
No. It is already known that type O people are at lower risk of disease, with higher risk to type B then higher still to type A then highest to type AB, and that when you do a GWAS study for associations with disease the ABO locus is one of exactly two loci that fall out as very important. The question is, is that due to some intrinsic degree of resistance to disease brought on by the ABO locus or is it due to this sort of transmission incompatibility? To know you need to figure out actual pairs of people you know transmitted to each other and see if particular pairwise patterns of blood types are more likely than others (which has never been done), and test the virions themselves to see that they can be neutralized by anti ABO antibody levels that you find in mucous membranes (though this is highly likely given previous work on other viruses).
Important to note that the author suggests that the best fit from observed blood type disease risk differences to a model like this would indicate that getting a virus from someone with an incompatible blood type would be about 40% as easy as getting infected from a compatible blood type.
One might be able to make arguments about intra-familial transmission versus extra-familial transmission rates with more math than I have time for right now.
In this model, if you ignore secretion status, type O people would be hardest to infect but most likely to spread. In the US about 45% of the population is type O, about 40% is type A, about 11% is type B, and about 4% is type AB according to the first source I found. You get the following fractions of the population being easy to transmit to and receive from for each blood type:
O—to 100%, from 45%
B—to 15%, from 56%
A—to 44%, from 85%
AB—to 4%, from 100%
If you assume that you are 40% as likely to spread to someone of a noncompatible blood type, you get a ease-of-infecting-others score for each type of: O = 100%, B = 49%, A = 66%, AB = 42%. Assuming you don’t know their secretion/nonsecretion status.
If you take into account non-secretors, then this is all slightly wrong and you actually have most non-O people slightly less infectious than that and some people who are A, B, or AB with their usual higher risk of getting infected but who transmit like type O. This is me—I am a type A nonsecretor and thus would be more vulnerable to transmission from a full 85% of the population, while being good at transmitting to 100% of the population. Such individuals might be more likely to be important nodes in the network.
If you look at the paper they show that the biggest result of this kind of an effect on an epidemiological model is that the more diverse the population is in terms of blood types—a more even distribution of A, B, and O—the slower spread happens, and the more homogenous a population is in terms of blood type the faster it happens regardless of which blood type is dominant.
So we can test AB-blood populations for antibodies and compare that to the general population, and you’ll know quickly if this theory is right or not?
No. It is already known that type O people are at lower risk of disease, with higher risk to type B then higher still to type A then highest to type AB, and that when you do a GWAS study for associations with disease the ABO locus is one of exactly two loci that fall out as very important. The question is, is that due to some intrinsic degree of resistance to disease brought on by the ABO locus or is it due to this sort of transmission incompatibility? To know you need to figure out actual pairs of people you know transmitted to each other and see if particular pairwise patterns of blood types are more likely than others (which has never been done), and test the virions themselves to see that they can be neutralized by anti ABO antibody levels that you find in mucous membranes (though this is highly likely given previous work on other viruses).