In human immunodeficiency virus (HIV) infection, functional defects and deletion of antigen-reactive T cells are more frequent than can be explained by direct viral infection. On culturing, both CD4+ and CD8+ T cells from asymptomatic HIV-infected individuals died as a result of programmed cell death (apoptosis). Apoptosis was enhanced by activation with CD3 antibodies. Programmed cell death, associated with impaired T cell reactivity, may thus be responsible for the deletion of reactive T cells that contributes to HIV-induced immunodeficiency.

Apoptosis (programmed cell death) can be difficult to detect in routine histological sections. Since extensive DNA fragmentation is an important characteristic of this process, visualization of DNA breaks could greatly facilitate the identification of apoptotic cells. We describe a new staining method for formalin-fmed, paraffii-embedded tissue sections that involves an in situ end-labeling (ISEL) procedure.

Differences in the in vivo and in vitro responses of T lymphocytes from chimpanzees and human subjects were compared for evidence of HIV‐1 related T‐cell dysfunction. There was no increased level of programmed cell death (PCD) in HIV‐1 infected chimpanzees in contrast to asymptomatic individuals. Anergy could be induced with HIV‐1 gp120 in human but not chimpanzee TH lymphocytes, however in vitro infection of chimpanzee TH cultures with HIV‐1 resulted in complete lysis of cells within three weeks. These findings suggest that the resistance of HIV‐1 infected chimpanzees to progression to AIDS is due to their relative resistance to the systemic effects of HIV‐1 on T‐cell dysfunction.

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