With exposure to bacterial antigen exacerbated in HIV infection via translocation and systemic dissemination of microbial products following mucosal barrier disruption, it remains unknown if this setting allows specific HIV-reactive CD8+ T cell populations to be influenced by microbes in an MHC-restricted context, and specifically, if MHC class I proteins can present microbial peptides that inflate specific subsets of memory HIV-specific T cell populations during active disease. Here, CD8A is linked to HIV infectious disease.