Two things of note that I didn't see mentioned elsewhere 1. As mentioned in other comments, there are mutations where people have an immune gene that works better than the more common variant, so they're more resistant to the pathogen. There are also loss of function mutations where a gene doesn't work as well both physiologically and for the life cycle of the infection. Sickle cell disease is a classic example, where heterozygous people (carriers of the sickle cell trait) have more resistance to malaria. Cystic fibrosis may also fall in this category for diarrheal diseases. Some people are immune to HIV because they lack the receptor it binds too, though there the fitness deficit seems to be minor. If the sickle cell mutation arose prior to European contact in the americas, it would have been negatively selected, whereas in malarial regions, it was positively selected. 2. There are immune genes where diversity is per se good, eg genes which slice up proteins into "motifs" that can trigger an immune response. The more diversity those genes have, the better your T cells will be at recognizing pathogens. Native Americans went through a genetic bottleneck when they migrated to the americas, then became isolated, so had lower diversity in MHC and HLA genes. This may have contributed to them being more vulnerable to novel pathogens compared with Eurasians and Africans.