A GWAS of a multiethnic cohort of HIV-1 controllers and progressors [93] obtained similar results as in the previous two studies [33,95] but with the added novelty that (1) the nature of the HLA-viral peptide interaction was the major factor modulating durable control of HIV infection, (2) HCP5 rs2395029-G was a proxy not only for HLA-B*57:01 but also for many protective and risk HLA alleles (predominantly at HLA-B), and (3) with an independent effect on HLA-C gene expression that together differentially affected the response to HIV and delayed progression to AIDS [106,107]. This evidence concerns the gene HCP5 and HIV infectious disease.