Yang XU, Chun-wei SHE, Xiao-yong ZHANG, Rong-juan PEI and Meng-ji LU. Interference of Hepatitis B Virus with Cellular Signaling*[J]. Virologica Sinica, 2008, 23(2): 100-106. doi: 10.1007/s12250-008-2940-0
Citation: Yang XU, Chun-wei SHE, Xiao-yong ZHANG, Rong-juan PEI, Meng-ji LU. Interference of Hepatitis B Virus with Cellular Signaling* .VIROLOGICA SINICA, 2008, 23(2) : 100-106.  http://dx.doi.org/10.1007/s12250-008-2940-0

乙型肝炎病毒干扰细胞内的信号传导*

  • 通讯作者: 陆蒙吉, mengji.lu@uni-due.de
  • 收稿日期: 2008-01-15
    录用日期: 2008-01-24
  • 乙型肝炎病毒的蛋白能影响细胞内的信号传导,引起细胞基因表达的改变。现有研究结果显示乙肝病毒的核衣壳蛋白和多聚酶蛋白的氨基末端片段(TP)能抑制干扰素的信号传导。此外,在肝癌细胞系中,乙肝病毒的复制和乙肝蛋白的表达能引起细胞基因表达的全局性改变。乙肝病毒的复制会引起细胞内干扰素刺激基因(ISGs)表达的异常调控,使用抗乙肝病毒的药物抑制病毒复制能部分恢复细胞内ISGs的表达调控。乙肝病毒的多聚酶末端蛋白(TP)能调节ISGs的表达,并能增强乙肝病毒的复制。乙肝病毒对细胞内信号传导的干扰调节作用在乙肝病毒的致病机制中可能占有重要地位。

Interference of Hepatitis B Virus with Cellular Signaling*

  • Corresponding author: Meng-ji LU, mengji.lu@uni-due.de
  • Received Date: 15 January 2008
    Accepted Date: 24 January 2008

    Fund Project: Deutsche Forschungsgemeinschaft Lu 669/5-1Deutsche Forschungsgemeinschaft Lu 669/2-1Deutsche Forschungsgemeinschaft GRK1045/1

  • The presence of hepatitis B virus (HBV) proteins leads to changes in the cellular gene expression. As a consequence, the cellular signaling processes are influenced by the actions of HBV proteins. It has been shown that HBV nucleocapsid protein and the amino-terminal part of polymerase termed as terminal protein (TP) could inhibit interferon signaling. Further, the global gene expression profiles differ in hepatoma cells with and without HBV gene expression and replication. The expression of interferon (IFN) stimulated genes (ISGs) was differently regulated in cells with HBV replication and could be modulated by antiviral treatments. The HBV TP has been found to modulate the ISG expression and enhance the HBV replication. The modulation of the cellular signaling processes by HBV may have significant implications for pathogenesis.

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    Interference of Hepatitis B Virus with Cellular Signaling*

      Corresponding author: Meng-ji LU, mengji.lu@uni-due.de
    • 1. Institut für Virologie, Universitätsklinikum Essen, Essen, 45122, Germany
    • 2. Department of Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China
    • 3. State Key Lab of Virology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430071, China
    • 4. Graduate School of the Chinese Academy of Sciences, Beijing, 100072, China
    Fund Project:  Deutsche Forschungsgemeinschaft Lu 669/5-1Deutsche Forschungsgemeinschaft Lu 669/2-1Deutsche Forschungsgemeinschaft GRK1045/1

    Abstract: The presence of hepatitis B virus (HBV) proteins leads to changes in the cellular gene expression. As a consequence, the cellular signaling processes are influenced by the actions of HBV proteins. It has been shown that HBV nucleocapsid protein and the amino-terminal part of polymerase termed as terminal protein (TP) could inhibit interferon signaling. Further, the global gene expression profiles differ in hepatoma cells with and without HBV gene expression and replication. The expression of interferon (IFN) stimulated genes (ISGs) was differently regulated in cells with HBV replication and could be modulated by antiviral treatments. The HBV TP has been found to modulate the ISG expression and enhance the HBV replication. The modulation of the cellular signaling processes by HBV may have significant implications for pathogenesis.