The immunopathogenesis of HBV infection.

The immunopathogenesis of HBV infection.
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DOI:
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发表时间:
1998
期刊:
影响因子:
1.2
通讯作者:
Koziel Mj
Koziel Mj
中科院分区:
医学4区
文献类型:
--
作者:
Koziel Mj

文献摘要

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摘要乙肝病毒感染的临床表现是病毒和宿主因素之间的平衡。对任何病毒的免疫反应包括对先天免疫和获得性病毒特异性免疫的协调防御。在急性乙肝中,与恢复相关的免疫反应包括针对乙肝病毒内多个表位的强大的多克隆CD4T细胞;针对表面包膜蛋白的抗体(抗-HBs),其发展需要存在CD4反应;以及乙肝病毒特异性细胞毒性T淋巴细胞(CTL)。乙肝病毒特异性CTL既能诱导感染的肝细胞死亡,又能产生细胞因子。大多数急性乙肝患者在没有大规模肝脏破坏的情况下恢复;这一点,加上转基因动物模型的证据,表明这些由T细胞产生的细胞因子在控制乙肝病毒复制方面发挥着重要作用。未能在急性乙肝病毒中做出有力反应的人会发展成慢性感染。在这些情况下,持续无效的免疫反应似乎是肝脏损伤的原因,并可能启动肝纤维化的过程。基于我们目前对急性和慢性乙肝免疫反应的了解,几个小组正在研究操纵慢性乙肝免疫反应的前景。
Abstract 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.