Similarly to HIV-1 infection, this study also associated HLA-B*57 with superior control of HCV, and HLA-B*35 with worse control, however there were no HLA-associated differences in spontaneous HCV clearance rates (Ruiz-Mateos et al., 2011), suggesting common host mechanisms involved in the control of plasma viremia in these two persistent viral infections. This evidence concerns the gene HLA-B and HIV-1 infection.