In conclusion, our data support a scenario in which the induction of IFNα/β during chronic HIV-1 infection exerts pathogenic instead of protective effects on host immunity by upregulating CD95 and Bak expression and sensitizing CD4+ T cells and CD8+ T cells to Fas-mediated apoptosis, but not to TRAIL or TNFα-induced death. The gene discussed is CD4; the disease is HIV-1 infection.