Fiore G, Jirillo E, Schiraldi O, Antonaci S
Dipartimento di Clinica Medica, Immunologia e Malattie Infettive, Università, Bari.
Recenti Prog Med. 1996 Jun;87(6):301-7.
The recent cloning and genomic identification of hepatitis C virus (HCV) by sensitive and specific immune techniques has allowed a better definition of both histopathological and clinical features of the previously not well defined non-A, non-B hepatitis. In this regard, antibodies to different HCV antigens are usually found during infection, even if some of them such as anti-E1 and anti-E2/NS1 have been shown to be associated with significant viraemic levels. Acute hepatitis C is self-limiting in a minority of cases only. Over 60% of acute hepatitis becomes in fact chronic and may progress towards cirrhosis. In about 10% of cases, hepatocellular carcinoma may develop in cirrhotic livers. The occurrence of a strict relationship between immunoresponsiveness and disease activity is suggested by the observation that peripheral blood mononuclear cell (PBMC) proliferation induced by NS3 structure is associated with self-limiting acute hepatitis, while PBMC stimulation by core antigen characterizes chronic C hepatitis. The demonstration of lymphoid aggregates, bile duct lesions, intraportal lymphocyte infiltration, increased adhesion molecule expression and augmented cytokine release clearly emphasizes the involvement of immune-mediated reactions in the development of liver damage, even if a direct cytopathic effect cannot be excluded. Finally, it is likely that HCV may favour, through immune-mediated mechanisms, autoantibody generation and/or the appearance of some extrahepatic autoimmune manifestations during the course of HCV chronic infection.
近期通过灵敏且特异的免疫技术对丙型肝炎病毒（HCV）进行克隆和基因组鉴定，使得之前定义不明确的非甲非乙型肝炎的组织病理学和临床特征得到了更好的界定。在这方面，感染期间通常会发现针对不同HCV抗原的抗体，即便其中一些抗体，如抗-E1和抗-E2/NS1，已被证明与显著的病毒血症水平相关。仅有少数急性丙型肝炎病例是自限性的。实际上，超过60%的急性丙型肝炎会转变为慢性肝炎，并可能进展为肝硬化。在约10%的病例中，肝硬化肝脏可能会发展为肝细胞癌。有观察表明，由NS3结构诱导的外周血单个核细胞（PBMC）增殖与自限性急性肝炎相关，而核心抗原刺激PBMC则是慢性丙型肝炎的特征，这提示免疫反应性与疾病活动之间存在紧密关系。淋巴样聚集、胆管病变、门脉内淋巴细胞浸润、黏附分子表达增加以及细胞因子释放增多的证实，明确强调了免疫介导反应在肝损伤发展过程中的作用，即便不能排除直接细胞病变效应。最后，HCV很可能通过免疫介导机制，在HCV慢性感染过程中促进自身抗体的产生和/或某些肝外自身免疫表现的出现。
