The relatively high incidence of infectious disease in alcoholics is attributed to the immunosuppressive effects of alcohol. The potential role of alcohol as cofactor in HIV infection and in the development and expression of AIDS is suggested but unknown. In order to understand better the contribution of alcohol to immune dysfunction following HIV infection, we assessed the presence of specific markers on thymus and spleen cells in C57B1/6 mice infected with LP-BM5 murine leukemia virus and fed ethanol-containing diets. In the first experiments, mice were fed diets containing 0, 4.5, 5.5, and 6% (v/v) ethanol for 14 weeks. High ethanol exposure (6%) resulted in severe dehydration and death after 7 weeks. Although moderately low intakes of ethanol did not significantly modify percentages of T and B cells, they increased the absolute number of mature T, B, and CD4+ cells and decreased percentages of Thy 1.2+ cells. In the second experiment, mice were infected with LP-BM5 murine leukemia retrovirus and fed diets containing 5% ethanol in a regimen of 5 days of ethanol diet and 2 days of diet without alcohol for 12 weeks. Ethanol exposure in the retrovirally infected mice showed a marked decrease in Thy 1.2+ (P < 0.05). Moderate decreases in percentages of CD4+, CD8+, CD5+ cells and an increase in Ia+ cells were also observed in the retrovirus/infected ethanol-treated mice. Moderate ethanol consumption during retroviral infection induced mild/moderate changes on lymphoid cells. Ethanol consumption may accelerate the progression of murine AIDS through such changes in the lymphoid cells of the spleen.