Infection of human thymic dendritic cells with HIV-1 induces the release of a cytotoxic factor(s).

Abstract

Lymphoid organs have been reported to represent the major site for the establishment and the propagation of human immunodeficiency virus (HIV-l) (1). HIV-1 infection is characterized by a permanent high-level of viral replication associated with a high-level turnover of CD4+ T cells (2). The late stages of the disease are characterized by a progressive depletion of CD4+ T cells that eventually lead to the development of the acquired immune deficiency syndrome (AIDS). A variety of direct and indirect mechanisms have been proposed to account for the decline of the CD4+ T cells (3). Among them, inappropriate activation of apoptosis, a programmed cell death process, has been proposed to contribute to the CD4+ T cell depletion (4). HIV-induced apoptotic cell death has been demonstrated not only in vitro but also in infected individuals and is now considered to be a major mechanism of HIV-mediated cell death (5–7).