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Acquired Immunodeficiency Syndrome (AIDS) was first reported in the United States in 1981 and has since become a major worldwide epidemic. The typical course of HIV disease begins with a primary infection followed by a relatively long latency phase and finally ends in the advance phase also called AIDS. There are two aspects considered the most important in HIV pathogenesis, namely viral replication and CD4+ T cell depletion. During the latency phase, tumor necrosis factor α (TNFα) has been shown to play a predominant role in HIV-1 replication and disease progression. Since ethanol is also an important risk factor and has been implicated in HIV-1 replication, we investigate the effects of ethanol on TNFα inducible signaling associated with HIV-1 replication in human CD4+ T cells. We demonstrate that clinically relevant ethanol concentrations significantly potentiate TNFα inducible NFκB. Although ethanol effectively collaborated with TNFα, by itself it does not have a direct effect on NFκΒ activation. The ethanol dependent potentiation of TNFα inducible NFκB nuclear translocation is observed to involve the enhanced degradation of IκBα. Additionally, the ethanol mediate