RELATIONSHIP OF HCV INFECTION & ALCOHOLIC LIVER DISEASE

慢性丙型肝炎患者抗丙型肝炎病毒抗体的检测 酒精性肝病(ALD)的发病率可能远远高于 普通人口。最近的证据表明，这在很大程度上是由于 这一人群中丙型肝炎病毒感染率的增加 而不是假阳性化验结果。此外，中国的丙型肝炎病毒感染 酗酒者可能与组织病理学上的晚期肝脏有关 疾病，提示丙型肝炎病毒在发展或进展中的作用 肝病在酒精者中的一个子集。 丙型肝炎病毒复制活动性与抗体应答的关系 ALD患者特征不佳；然而，在患有ALD的患者中 酒精性肝病，可能有相当数量的 不能产生可检测到的抗-丙型肝炎病毒的慢性感染者 抗体。目前尚不清楚ALD诱导的免疫抑制是什么作用 发挥抑制抗-丙型肝炎病毒抗体反应的作用。 我们建议使用聚合酶链式反应分析，抗丙型肝炎病毒EIA，和重组 免疫印迹试验(RIBA)抗丙型肝炎病毒确证试验研究 丙型肝炎患者丙型肝炎病毒感染情况及其抗体反应 和ALD一起。我们建议研究风险因素在 使用ALD进行开发。我们进一步建议调查 酒精性肝病对丙型肝炎病毒感染的免疫抑制作用 测量伴有ALD和丙型肝炎的受试者的比例 未能产生可测量的抗丙型肝炎病毒抗体的感染，通过测量 丙型肝炎病毒抗体阳性与阴性患者的病毒滴度 对丙型肝炎病毒的反应，并通过测量体外B细胞反应 商陆有丝分裂原及其在体内的原发和继发反应 乙肝表面抗原在同一受试者组中。结果来自 这些研究将使我们能够更好地理解 酒精性肝病的发展，有助于阐明酒精性肝脏的作用 疾病诱导的免疫抑制在调节抗体反应中的作用 与丙型肝炎病毒感染有关。

The prevalence of anti-hepatitis C virus (HCV) antibody in patients with alcoholic liver disease (ALD) may be much higher than that of the general population. Recent evidence suggests that this is largely due to a increase in the prevalence of HCV infection in this population rather than false positive assay results. Furthermore, HCV infection in alcoholics may be associated with histopathologically advanced liver disease, suggesting a role for HCV in the development or progression of liver disease in a subset alcoholics. The relationship of antibody response to active HCV replication in patients with ALD is poorly characterized; however, in patients with alcoholic liver disease, there may be a significant number of chronically infected individuals who fail to produce detectable anti-HCV antibody. It is not yet known what role ALD-induced immune suppression plays in the suppression of anti-HCV antibody response. We propose to use a PCR assay, an anti-HCV EIA, and a recombinant immunoblot assay (RIBA) anti-HCV confirmatory test to study the prevalence of HCV infection and the antibody response to it in patients with ALD. We propose to study the role of risk factors in the development with ALD. We further propose to investigate the effects of alcoholic liver disease-induced immune suppression on HCV infection: by measuring the proportion of subjects with concomitant ALD and HCV infection who fail to produce measurable anti-HCV antibody, by measuring the HCV viral titer in subjects with and without measurable antibody response to the HCV virus, and by measuring the in vitro B-cell response to pokeweed mitogen and the in vivo primary and secondary responses to hepatitis B surface antigen in the same subject groups. Results from these studies will allow us to better understand potentiating factors in the development of ALD and will help clarify the role of alcoholic liver disease-induced immune suppression in modulating the antibody response to HCV infection.