Ethanol as a possible cofactor in the development of murine AIDS.

Abstract

Chronic ethanol (EtOH) abuse in humans leads to a variety of immunomodulatory events that can alter resistance to a number of infectious agents. Whether alcohol abuse affects the susceptibility to human immunodeficiency virus infection or the subsequent development of acquired immune deficiency syndrome (AIDS) is a matter of extreme importance; however, available information in humans or animal models is limited. The goal of this study was to evaluate the effect of chronic EtOH feeding in mice on the development of immunodeficiency in the murine model of AIDS (MAIDS). C57BI/6 mice were placed on the Lieber-DeCarli liquid EtOH diet (25% or 31% total caloric intake) or a nutrient-matched isocaloric liquid control diet. Seven days later, mice were infected with the LP-BM5 murine leukemia virus mixture, and groups of infected and noninfected mice were assayed at defined time points postinfection for antigen-specific and nonspecific immune responses. In the absence of retroviral infection, chronic EtOH feeding (5-8 weeks) led to reductions in spleen weights, compared with isocaloric controls. In spite of reduced spleen size, mitogenic responses of spleen cells to concanavalin A (ConA) and lipopolysaccharide (LPS) were elevated in EtOH-fed mice, as compared with mice fed the control diet. Chronic EtOH feeding also enhanced the allogeneic mixed lymphocyte response and increased antigen-specific priming of both B-cells and CD4+ T-cells to the antigen, sheep red blood cells. In MAIDS-infected mice, chronic EtOH feeding delayed but did not prevent the onset of virus-induced immunodeficiency and MAIDS-induced autoantibody synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)