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Oxidative stress in human immunodeficiency virus infection
N Israël1, M A Gougerot-Pocidalo
1Unité de Biologie des Rétrovirus, Institut Pasteur, Paris, France. nisrael@pasteur.fr
Cellular and Molecular Life Sciences : CMLS
|February 3, 1998
Summary
Human immunodeficiency virus (HIV-1) infection causes inflammation and oxidative stress. This stress contributes to CD4+ T lymphocyte depletion and enhances HIV transcription, suggesting antioxidants as potential therapies.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human immunodeficiency virus (HIV-1) infection leads to chronic inflammation, characterized by elevated inflammatory cytokines and reactive oxygen intermediates (ROIs).
- Activated polymorphonuclear neutrophils and the viral Tat protein are early sources of ROIs during HIV infection.
Purpose of the Study:
- To review the effects of oxidative stress on immune response, T lymphocyte survival, and HIV transcription/replication.
- To understand oxidative stress's role in HIV pathophysiology and explore antioxidant therapy potential.
Main Methods:
- Review of ex vivo and in vitro experimental data.
- Analysis of biological parameters including immune response, T lymphocyte apoptosis, and viral transcription.
Main Results:
- Oxidative stress contributes to CD4+ T lymphocyte depletion via increased apoptosis, particularly Fas-induced apoptosis.
- Oxidative stress facilitates NF-kappa B-dependent HIV transcription and may promote early HIV activation from a quiescent state.
- Established HIV replication is not significantly influenced by this oxidative stress.
Conclusions:
- Oxidative stress is a key factor in HIV-1 pathophysiology, impacting immune cells and viral activity.
- Antioxidant molecules show potential as therapeutic agents for acquired immunodeficiency syndrome (AIDS).