Cellular and Molecular Life Sciences CMLS

, Volume 53, Issue 11, pp 864–870

Oxidative stress in human immunodeficiency virus infection

  • N. Israël
  • M.-A. Gougerot-Pocidalo

DOI: 10.1007/s000180050106

Cite this article as:
Israël, N. & Gougerot-Pocidalo, M. CMLS, Cell. mol. life sci. (1997) 53: 864. doi:10.1007/s000180050106

Abstract.

Infection by the human immunodeficiency virus (HIV-1) causes chronic ongoing inflammation in HIV-1 seropositive individuals as shown by high plasma levels of inflammatory cytokines and production of reactive oxygen intermediates (ROIs). One source of ROIs is provided from the very early stages of HIV infection by activated polymorphonuclear neutrophils. Tat, the viral protein, is also specifically responsible for an endogenous cellular increase of ROI. In this review we also evaluate the effects of this oxidative stress on various biological parameters such as immune response and survival of T lymphocytes, virus transcription and replication. It was clearly demonstrated in ex vivo experiments that the oxidative stress due to infection itself participates in CD4+ T lymphocyte depletion by increasing their rate of apoptosis and particularly of Fas-induced apoptosis. This oxidative stress also facilitates NF-κB-dependent activation of HIV transcription. In vitro studies suggest that the early steps of HIV activation from its quiescent state might be subsequently facilitated by this oxidative environment, whereas already active replication is not influenced. The data presented here lead to a better understanding of the consequences of oxidative stress on the pathophysiology of HIV infection and also enable us to evaluate the potential use of antioxidant molecules as therapeutic agents against AIDS.

Key words. Oxidative stress; HIV infection; HIV replication; HIV transcription; antioxidants.

Copyright information

© Birkhäuser Verlag Basel, 1997

Authors and Affiliations

  • N. Israël
    • 1
  • M.-A. Gougerot-Pocidalo
    • 2
  1. 1.Unité de Biologie des Rétrovirus, Institut Pasteur, 28 rue du Dr Roux, F-75724 Paris Cedex 15 (France), e-mail: nisrael@pasteur.frFR
  2. 2.Unité INSERM U 294, Hôpital Bichat, 46 rue Henri Huchand, F-75018 Paris (France)FR