Alcohol consumption alters cytokine release during murine AIDS

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a human immunodeficiency virus (HIV), representing the end point in a progressive sequence of immunosuppressive changes. HIV, the key causative agent of AIDS, induces immunosuppression that render the body highly susceptible to opportunistic infections and neoplasm. However, the onset of clinical symptoms of AIDS (e.g., 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 alcohol (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 HIV infection, and subsequently accelerate the development of AIDS. The purpose of this review is to present evidence of EtOH-induced cytokine dysregulation during murine AIDS. Our results done in murine AIDS indicate that EtOH consumption may accelerate the development of AIDS by disrupting cytokine production. These EtOH-induced abnormalities in cytokine release may promote a more rapid development of AIDS as a cofactor, which exacerbates the immune dysfunctions initiated by retrovirus infection.