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乙型肝炎病毒的分子病毒学。

The molecular virology of hepatitis B virus.

机构信息

Institute of Medical Virology, National Reference Centre for Hepatitis B and D Viruses, Justus-Liebig University of Giessen, Giessen, Germany.

出版信息

Semin Liver Dis. 2013 May;33(2):103-12. doi: 10.1055/s-0033-1345717. Epub 2013 Jun 8.

DOI:10.1055/s-0033-1345717
PMID:23749666
Abstract

Hepatitis B virus (HBV) is one of the smallest enveloped DNA viruses and the prototype member of the family of Hepadnaviridae that causes acute and chronic infections of mammals (including human) and birds. HBV has evolved an extreme adaptation and dependency to differentiated hepatocytes of its host. Despite its very limited coding capacity with only four open-reading frames, HBV is able to evade the immune system of the host and persist lifelong within infected hepatocytes. During active replication, HBV produces enormous viral loads in the blood and a massive surplus of subviral surface antigen particles in the serum of infected patients without killing their hepatocytes. Together with the use of a reverse transcriptase during replication, it provides an enormous genetic flexibility for selection of viral mutants upon selective pressure, for example, by the immune system or antiviral therapy. In addition, viral wild-type and mutated genomes are stably archived in the nucleus of the infected hepatocyte in an episomal DNA form that provides independence from cellular replication or integration within the host genome. We are just beginning to understand the delicate molecular and cellular interactions during the HBV replicative cycle within infected hepatocytes, so further studies are urgently needed to provide a better basis for further diagnostic and therapeutic options.

摘要

乙型肝炎病毒 (HBV) 是最小的包膜 DNA 病毒之一,也是家族 Hepadnaviridae 的原型成员,可引起哺乳动物(包括人类)和鸟类的急性和慢性感染。HBV 已经进化出一种极端的适应性和对其宿主分化肝细胞的依赖性。尽管其编码能力非常有限,只有四个开放阅读框,但 HBV 能够逃避宿主的免疫系统,并在感染的肝细胞内终身存在。在活跃复制期间,HBV 在血液中产生大量的病毒载量,并在感染患者的血清中产生大量亚病毒表面抗原颗粒,而不会杀死其肝细胞。与复制过程中使用逆转录酶一起,它为病毒突变体的选择提供了巨大的遗传灵活性,例如,通过免疫系统或抗病毒治疗。此外,病毒野生型和突变型基因组以游离体 DNA 形式稳定地存档于感染肝细胞的核内,从而使其独立于细胞复制或整合到宿主基因组中。我们才刚刚开始了解感染肝细胞中 HBV 复制周期期间的微妙分子和细胞相互作用,因此迫切需要进一步的研究,为进一步的诊断和治疗选择提供更好的基础。

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