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HBx 在乙型肝炎病毒持续感染中的作用及其治疗意义。

Role of HBx in hepatitis B virus persistence and its therapeutic implications.

机构信息

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, United States.

Department of Biochemistry and Molecular Biology, Drexel University College of Medicine, Philadelphia, PA 19102, United States.

出版信息

Curr Opin Virol. 2018 Jun;30:32-38. doi: 10.1016/j.coviro.2018.01.007. Epub 2018 Feb 20.

DOI:10.1016/j.coviro.2018.01.007
PMID:29454995
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5988931/
Abstract

Chronic hepatitis B virus infection is a significant risk factor for cirrhosis and hepatocellular carcinoma. The HBx protein is required for virus replication, but the lack of robust infection models has hindered our understanding of HBx functions that could be targeted for antiviral purposes. We briefly review three properties of HBx: its binding to DDB1 and its regulation of cell survival and metabolism, to illustrate how a single viral protein can have multiple effects in a cell. We propose that different functions of HBx are needed, depending on the changing hepatocyte environment encountered during a chronic virus infection, and that these functions might serve as novel therapeutic targets for inhibiting hepatitis B virus replication and the development of associated diseases.

摘要

慢性乙型肝炎病毒感染是肝硬化和肝细胞癌的重要危险因素。HBx 蛋白是病毒复制所必需的,但缺乏强大的感染模型阻碍了我们对 HBx 功能的理解,这些功能可能成为抗病毒的靶点。我们简要回顾了 HBx 的三个特性:它与 DDB1 的结合及其对细胞存活和代谢的调节,以说明单个病毒蛋白如何在细胞中产生多种效应。我们提出,HBx 的不同功能取决于在慢性病毒感染过程中遇到的不断变化的肝细胞环境,并且这些功能可能成为抑制乙型肝炎病毒复制和相关疾病发展的新的治疗靶点。

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本文引用的文献

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Identifying and Characterizing Interplay between Hepatitis B Virus X Protein and Smc5/6.鉴定和表征乙型肝炎病毒X蛋白与Smc5/6之间的相互作用
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Hepatitis B virus X protein is capable of down-regulating protein level of host antiviral protein APOBEC3G.乙型肝炎病毒 X 蛋白能够下调宿主抗病毒蛋白 APOBEC3G 的蛋白水平。
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The Smc5/6 Complex Restricts HBV when Localized to ND10 without Inducing an Innate Immune Response and Is Counteracted by the HBV X Protein Shortly after Infection.当定位于ND10时,Smc5/6复合物可限制乙肝病毒,且不诱导先天免疫反应,感染后不久即被乙肝病毒X蛋白抵消。
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