Consistent with anti-Gag (particularly p24) CD8+ T-cell responses as key determinants of HIV control61,64–67, we previously identified two highly significant B*39:02-associated polymorphisms in Gag (at codons 315 and 319, both in p24) and three in Pol (at codons 70 and 79 in protease, and 322 in reverse transcriptase)40, suggesting strong and reproducible targeting of these regions by B*39:02-restricted T-cell responses as possible determinants of B*39:02-mediated HIV control, where such effects remain detectable into chronic HIV-1 infection. This evidence concerns the gene CD8A and HIV-1 infection.