In the context of HIV-1 infection, this in principle allows them to (i) be primed by autologous human monocytes and dendritic cells presenting HIV-1 peptides in the context of MHC, (ii) recognize MHC-presented HIV-1 peptides on HIV-1 infected CD4+ T cells, and (iii) engage with and prime cognate B cells to class switch, undergo affinity maturation, and produce anti-HIV-1 antibodies. This evidence concerns the gene HLA-C and HIV-1 infection.