Ferri S, Muratori L, Lenzi M, Granito A, Bianchi F B, Vergani D
Institute of Liver Studies, King's College School of Medicine at King's College Hospital, Denmark Hill, London, UK.
Curr Pharm Des. 2008;14(17):1678-85. doi: 10.2174/138161208784746824.
Hepatitis C virus (HCV) infection is characterized by a number of autoreactive manifestations, such as autoantibody production, cryoglobulinemia and thyroid disorders. We will analyse critically the mechanisms invoked, and partially documented, to explain such manifestations arising in genetically predisposed individuals exposed to HCV. In particular we will examine the available evidence implicating the virus in lowering the B cell activation threshold, in directly infecting lymphocytes and in inducing self-reactivity through a mechanism of molecular mimicry. We will then move to the HCV related clinical immunopathological manifestations, with a specific attention to the effects of antiviral treatment.
丙型肝炎病毒（HCV）感染的特征是出现多种自身反应性表现，如自身抗体产生、冷球蛋白血症和甲状腺疾病。我们将严格分析为解释在遗传易感性个体中接触HCV后出现的此类表现而提出的、部分有文献记载的机制。特别是，我们将研究现有证据，这些证据表明该病毒在降低B细胞激活阈值、直接感染淋巴细胞以及通过分子模拟机制诱导自身反应性方面所起的作用。然后，我们将转向与HCV相关的临床免疫病理表现，并特别关注抗病毒治疗的效果。
