Activation-associated necrosis in human immunodeficiency virus infection

J Infect Dis. 1999 Feb;179(2):352-60. doi: 10.1086/314594.

Abstract

Mitogenic stimulation of lymphocytes from persons infected with human immunodeficiency virus (HIV) resulted in massive cell death. In addition to early apoptosis, a second wave of cell death occurred 48-72 h after stimulation. At that time, the cells were enlarged, leaked content, and had plasma membrane damage-all indicative of necrosis. Furthermore, DNA fragmentation as determined by TUNEL assay was virtually absent. This activation-associated necrosis could not be prevented by interfering with CD95/CD95-ligand interactions or by blocking caspase activity and was unaffected by neutralizing antibodies to tumor necrosis factor-alpha or interferon-gamma. Necrosis was also induced by activation of normal lymphocytes in the presence of ribavirin, which inhibits the de novo pathway of nucleotide synthesis. Lymphocytes from HIV-infected persons are defective in their ability to synthesize nucleotides via this pathway, indicating one possible mechanism for the activation-associated necrosis seen in HIV infection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis
  • CD3 Complex / analysis
  • CD3 Complex / immunology
  • CD5 Antigens / analysis
  • CD5 Antigens / immunology
  • Cell Count
  • Cytokines / immunology
  • Cytokines / pharmacology
  • HIV Infections / immunology
  • HIV Infections / pathology*
  • Humans
  • Lymphocyte Activation*
  • Lymphocytes / immunology
  • Lymphocytes / pathology*
  • Male
  • Middle Aged
  • Necrosis
  • Nucleotides / biosynthesis

Substances

  • CD3 Complex
  • CD5 Antigens
  • Cytokines
  • Nucleotides