This study was supported by the National Institutes of Health Grant AA23497. E.A.F. was supported by the National Institutes of Health Training Fellowship AA05341.
Ethanol as a Possible Cofactor in the Development of Murine AIDS
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 19, Issue 4, pages 915–922, August 1995
How to Cite
Fitzpatrick, E. A., Rhoads, C. A., Espandiari, P., Kaplan, A. M. and Cohen, D. A. (1995), Ethanol as a Possible Cofactor in the Development of Murine AIDS. Alcoholism: Clinical and Experimental Research, 19: 915–922. doi: 10.1111/j.1530-0277.1995.tb00967.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication May 30, 1994; accepted March 2, 1995
- Immune Response;
Chronic ethanol (EtOH) abuse in humans leads to a variety of immuno-modulatory 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). C57BV6 mice were placed on the Lieber-DeCarli liquid EtOH diet pS% or 31% total caloric intake) or a nutrient-matched isocaloric Quid control diet. Seven days later, mice were infected with the LP-BMS 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. In contrast to mice with MAIDS infection alone, infected mice fed an EtOH diet displayed significant mitogenic responses to ConA and LPS at 4 weeks postinfection; however, at 8 weeks postinfection, both groups were completely immunosuppressed. Liver damage was detected in all groups of EtOH-fed mice, as indicated by the elevated liver enzymes, ALT and‘ASR moreover, MAIDS infection did not alter the extent of liver damage caused by EtOH feeding. These data suggest that chronic feeding of the Lieber-DeCarli EtOH diet in mice can lead to immune enhancement and that under these conditions causes a delay in the onset of MAIDS. Whether these results are caused by the effects of chronic exposure of the immune system to EtOH or to elevated Went levels in the standard Lieber-DeCarli liquid EtOH diet is discussed.