P revailing views concerning the pathogenic mechanisms of AIDS have shifted from models that focus primarily on direct HIV-mediated killing of CD4⁺ T cells to models that emphasize the pathogenic role of generalized immune system activation. The observation that increases in T cell turnover seen in HIV-infected individuals primarily reflect increased proliferation of effector-memory T cells supports the concept that chronic immune activation plays a prominent, if not predominant, role in the pathogenesis of AIDS.