Is alcohol consumption a cofactor in the development of acquired immunodeficiency syndrome?

Excessive alcohol (EtOH) consumption and acquired immunodeficiency syndrome (AIDS) are two major public health problems in the United States. Overwhelming evidence is showing that heavy EtOH ingestion broadly suppresses the various arms of immune response, seriously impairing the body's normal host defense to invading microbes and tumorigenesis. The onset of clinical symptoms of AIDS (low CD4+ T cells count, opportunistic infections, and tumors) is quite variable among HIV+ individuals with a mean incubation time 3-10 years following seroconversion. Because of the deleterious effects of chronic EtOH consumption on cytokine release, immune response, host defense, nutritional status, and oxidative stress, it has been believed to be a possible cofactor that could enhance the host's susceptibility to infections, and subsequently increase the rate of AIDS development. The purpose of this review is to present evidence indicating clinical disorders during EtOH ingestion in murine AIDS. These EtOH-induced abnormalities may promote a more rapid development of AIDS in HIV-infected individuals.

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