ROLE OF ALCOHOL IN THE DEVELOPMENT OF AIDS

酒精在HIV感染和感染中作为辅助因素的潜在作用 流行病学提示艾滋病的发展 研究，但酒精影响的实验证据是 由于缺乏，我们分离了外周血单个核细胞(PBM) 取自6名正常志愿者40盎司前后的细胞。一桶啤酒 L(1.2)或其他酒精中乙醇的等量剂量 饮料。这些细胞在体外暴露于HIV病毒。 术后对感染的抵抗力显著下降。 酒精摄入量通过形成突触的数量来评估(p <0.001)和外周血中释放的P24抗原水平 培养(p<0.001)。未感染的培养已完成 同时也表明，饮酒也会降低 淋巴细胞产生IL-2和IL-2的能力 可溶性免疫反应抑制因子(SIRS)(p< 0.001)，预先合成辅助和抑制T细胞， 分别进行了分析。我们的数据强烈表明，伴随而来的是 酗酒和通过性行为接触病毒或b 药物滥用中使用的受感染针头可能通过以下方式增强传染性 爱滋病毒。 下面的具体目标不是相互排斥的，将 有助于进一步阐明潜在的细胞和 导致随后减少的体液事件 宿主对HIV的抵抗力。 1.进一步阐明酒精诱导的大鼠脑内神经递质增加。 人外周血单核细胞的易感程度 从正常受试者的细胞到HIV感染。酒精量 其对免疫系统的不良影响的消耗和持续时间 将对系统进行检查。 2.阐明乙醇诱导的潜在机制 细胞和体液水平的免疫调节。 3.寻找诱因(如淋巴因子、单核细胞因子、各种 增长因素等)这可能中和或逆转 乙醇引起的不良反应。

The potential role of alcohol as a cofactor in HIV infection and development of AIDS has been suggested by epidemiologic studies, but experimental evidence for the effect of alcohol is lacking, we isolated the peripheral blood mononuclear (PBM) cells from six normal volunteers before and after 40 oz. of beer (1.2 L) or the equivalent dose of ethanol in other alcoholic beverages. These cells were exposed in vitro to HIV virus. There was a significant decrease of resistance to infection after alcohol ingestion as assessed by the number of synctia formed (p less than 0.001) and levels of P24 antigen released in PBM cultures (p less than 0.001). Noninfected cultures done simultaneously showed that alcohol ingestion also decreased the abiltity of lymphocytes to produce interleukin 2 (IL-2) and soluble immune response suppressor factor (SIRS) (p less than 0.001), synthesized preminiarly be helper and suppressor T cells, respectively. Our data strngly suggest that the concomitant use fo alcohol and exposure to the virus through sexual activity or b infected needles used in drug abuse may enhance infectivity by HIV. The Specific Aims below are not mutually exclusive and will contribute towards further elucidation of underlying cellular and humoral events which result in subsequent decrease in the resistance of host to HIV. 1. To further elucidate the alcohol-induced increase in the degree of susceptibility of human peripheral blood mononuclear cells from normal subjects to HIV infection. Amount of alcohol consumption and duration of its adverse effect on the immune system will be examined. 2. To elucidate the underlying mechanisms of ethanol induced immunomodulation at cellular and humoral levels. 3. To seek out agents (e.g., lymphokines, monokines, various growth factors etc.) which might neutralize or reverse the adverse effects induced by ethanol.