Reactive Oxygen Species, Antioxidants, and Acquired Immunodeficiency Syndrome

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Abstract
A cquired immunodeficiency syndrome (AIDS) results from A infection with a human immunodeficiency virus (HIV-1 or HIV-2) that eventually destroys a specific subset (CD4+) of helper T lymphocytes, so that the patient ultimately succumbs to opportunistic infections and/or certain neoplasms.1 A high proportion of, and perhaps all, HIV-seropositive patients will show disease progression. Thus, of a cohort of HIV-1—positive subjects who were followed up for 3 years, 19% developed AIDS-related complex (ARC) and 26% developed AIDS.2 Also, 41% of those who remained asymptomatic showed laboratory evidence of decline of immunologic status.2 The only drug currently approved for the treatment of AIDS is 3'-azido-3'-deoxythymidine (azidothymidine, or AZT, now called zidovudine), which is therapeutically effective but has significant time- and dose-related toxicity.3,4 Recent reports have implicated reactive oxygen species both in the pathogenesis of HIV infection and in some of the side effects of drugs such as zidovudine.