CD8A and HIV infectious disease: Such mechanisms may also be in place during HIV infection where genetic [55] or functional [56–58] evidences suggest a role in the variation of NK cell functions for resistance or susceptibility to the development of AIDS, where detrimental effects of excessive levels of IFN-α/β [59] or of pro-inflammatory cytokines [60,61] have been recently suggested, and where the initiation of antiviral CD8 T cell responses appears delayed [62–64].