Taken as a whole, such strikingly disparate effects of HLA-B alleles on the two outcome measures (control of VL and susceptibility to infection) in the same cohort imply that if HLA-B alleles play any substantial role in modulating resistance or susceptibility to infection, the convincingly documented mechanism by which those alleles mediate CTL response to specific viral epitopes during the course of subtype C infection is unlikely to represent the dominant mechanism regulating heterosexual acquisition. Here, HLA-B is linked to infection.