The Hepatitis B Virus X Protein Disrupts Innate Immunity by Downregulating Mitochondrial Antiviral Signaling Protein

DOI PDF 被引用文献13件
  • Congwen Wei
    Beijing Institute of Biotechnology , Changchun ,
  • Caifei Ni
    Beijing Institute of Biotechnology , Changchun ,
  • Ting Song
    Beijing Institute of Biotechnology , Changchun ,
  • Yu Liu
    The General Hospital of Chinese People’s Armed Police Forces , Changchun ,
  • XiaoLi Yang
    The General Hospital of Chinese People’s Armed Police Forces , Changchun ,
  • Zirui Zheng
    Beijing Institute of Biotechnology , Changchun ,
  • Yongxia Jia
    Beijing Institute of Biotechnology , Changchun ,
  • Yuan Yuan
    Beijing Institute of Biotechnology , Changchun ,
  • Kai Guan
    Beijing Institute of Biotechnology , Changchun ,
  • Yang Xu
    Key Laboratory for Molecular Enzymology and Engineering, JiLin University , Changchun ,
  • Xiaozhong Cheng
    Beijing Institute of Biotechnology , Changchun ,
  • Yanhong Zhang
    Beijing Institute of Biotechnology , Changchun ,
  • Xiao Yang
    Beijing Institute of Biotechnology , Changchun ,
  • Youliang Wang
    Beijing Institute of Biotechnology , Changchun ,
  • Chaoyang Wen
    Chinese People's Liberation Army General Hospital , Beijing ,
  • Qing Wu
    Chinese People's Liberation Army General Hospital , Beijing ,
  • Wei Shi
    Key Laboratory for Molecular Enzymology and Engineering, JiLin University , Changchun ,
  • Hui Zhong
    Beijing Institute of Biotechnology , Changchun ,

書誌事項

公開日
2010-07
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.0903874
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Previous studies have shown that both hepatitis A virus and hepatitis C virus inhibit innate immunity by cleaving the mitochondrial antiviral signaling (MAVS) protein, an essential component of the virus-activated signaling pathway that activates NF-κB and IFN regulatory factor-3 to induce the production of type I IFN. For human hepatitis B virus (HBV), hepatitis B s-Ag, hepatitis B e-Ag, or HBV virions have been shown to suppress TLR-induced antiviral activity with reduced IFN-β production and subsequent induction of IFN-stimulated genes. However, HBV-mediated suppression of the RIG-I–MDA5 pathway is unknown. In this study, we found that HBV suppressed poly(deoxyadenylate-thymidylate)-activated IFN-β production in hepatocytes. Specifically, hepatitis B virus X (HBX) interacted with MAVS and promoted the degradation of MAVS through Lys136 ubiquitin in MAVS protein, thus preventing the induction of IFN-β. Further analysis of clinical samples revealed that MAVS protein was downregulated in hepatocellular carcinomas of HBV origin, which correlated with increased sensitivities of primary murine hepatocytes isolated from HBX knock-in transgenic mice upon vesicular stomatitis virus infections. By establishing a link between MAVS and HBX, this study suggests that HBV can target the RIG-I signaling by HBX-mediated MAVS downregulation, thereby attenuating the antiviral response of the innate immune system.</jats:p>

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