In summary, our data indicate that variation according to individual HLA-A, -B and –C alleles in HESNs and, by implication, whatever differential CTL responses may be mediated by those different alleles, fail to explain much if any variation in resistance to infection among Zambian partners exposed to HIV-1 subtype C. Of course, these disparate results for individual alleles do not preclude possible contributions of class I molecules by any of several alternative mechanisms. This evidence concerns the gene HLA-A and infection.