Abstract
Human immunodeficiency virus (HIV-1) is the etiologic agent of acquired immunodeficiency syndrome (AIDS). Our understanding of the complexities of pathogenic mechanisms of HIV disease is still evolving; however, the mechanism whereby HIV-1 infection leads to profound depletion of CD4 T cells remains one of the central unsolved problems in AIDS research. In the past several years, there has been a dichotomy between virological and immunological viewpoints in understanding HIV-mediated cytopathicity, the former emphasizing killing of infected CD4 cells by HIV and the latter emphasizing indirect mechanisms wherein HIV or its soluble component(s) alter CD4 T-cell function and induce susceptibility to apoptosis.