Koziel M J
Harvard Institute of Medicine, Beth Israel Deaconness Medical Center, Boston, Massachusetts, USA.
Antivir Ther. 1998;3(Suppl 3):13-24.
Clinical manifestations of hepatitis B virus (HBV) infection are a balance between viral and host factors. The immune response against any virus consists of a coordinated defence of innate immunity and acquired, virus-specific immunity. In acute HBV, immune responses associated with recovery include vigorous, polyclonal CD4 T cells directed against multiple epitopes within HBV; antibodies directed against surface envelope proteins (anti-HBs), the development of which requires the presence of a CD4 response; and HBV-specific cytotoxic T lymphocytes (CTLs). HBV-specific CTLs can induce death of infected hepatocytes as well as produce cytokines. Most individuals with acute HBV recover without evidence of massive liver destruction; this, plus evidence from transgenic animal models, suggests that these cytokines produced by T cells play an important role in controlling HBV replication. Individuals who fail to mount a vigorous response in acute HBV develop chronic infection. In these cases, the persisting ineffective immune response appears to be responsible for liver damage and is likely to initiate the process of hepatic fibrosis. Based on our current understanding of the immune response in acute and chronic HBV, several groups are investigating the prospect of manipulating the immune response in chronic HBV.
乙型肝炎病毒（HBV）感染的临床表现是病毒因素与宿主因素之间的平衡。针对任何病毒的免疫反应都包括固有免疫和获得性病毒特异性免疫的协同防御。在急性HBV感染中，与康复相关的免疫反应包括针对HBV内多个表位的强烈多克隆CD4 T细胞；针对表面包膜蛋白的抗体（抗-HBs），其产生需要存在CD4反应；以及HBV特异性细胞毒性T淋巴细胞（CTL）。HBV特异性CTL可诱导受感染肝细胞死亡并产生细胞因子。大多数急性HBV感染者康复后无大量肝组织破坏的迹象；这一点以及转基因动物模型的证据表明，T细胞产生的这些细胞因子在控制HBV复制中起重要作用。在急性HBV感染中未能产生强烈反应的个体则会发展为慢性感染。在这些情况下，持续存在的无效免疫反应似乎是肝损伤的原因，并且很可能启动肝纤维化过程。基于我们目前对急性和慢性HBV免疫反应的理解，几个研究小组正在研究调控慢性HBV免疫反应的前景。
