The role of oxidative stress in disease progression in individuals infected by the human immunodeficiency virus.
This review describes the potential role of oxidative stress as a cofactor of disease progression from asymptomatic human immunodeficiency virus (HIV) infection to the acquired immunodeficiency syndrome (AIDS). Oxidative stress is a known activator of HIV replication in vitro through the activation of a factor that binds to a DNA-binding protein, NF-kappa B, which in turn stimulates HIV gene expression by acting on the promoter region of the viral long terminal repeat. Tumor necrosis factor alpha (TNF-alpha), an essential cytokine produced by activated macrophages, is also involved in the activation of HIV infection through similar mechanisms. TNF-mediated cytotoxicity of cells exposed to this substance is related to the generation of intracellular hydroxyl radicals. An indirect argument in favor of the role of oxidative stress in HIV-associated disease progression is the consumption of glutathione (GSH), a major intracellular antioxidant, during HIV infection and progression. GSH is known to play a major role in regulation of T cell immune functions. Oxidative stress may also play an important role in the genesis of cellular DNA damage and, in this context, may be related to HIV-associated malignancies and disease progression. Finally, the role of antioxidants as components of therapeutic strategies to combat HIV disease progression is discussed.
Baruchel
S
S
Department of Pediatrics, Montreal Children's Hospital, Quebec, Canada.
Wainberg
M A
MA
D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology* / Q000378:metabolism; D005609:Free Radicals; D006801:Humans; D016877:Oxidants / Q000494:pharmacology; D010084:Oxidation-Reduction; D013312:Stress, Physiological / Q000378:metabolism
D005609:Free Radicals; D016877:Oxidants