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首页> 外文期刊>AIDS Research and Human Retroviruses >Human Immunodeficiency Virus Coinfection with Hepatitis B Virus Leads to a Decrease in Extracellular and Intracellular Hepatitis B Antigen
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Human Immunodeficiency Virus Coinfection with Hepatitis B Virus Leads to a Decrease in Extracellular and Intracellular Hepatitis B Antigen

机译：用乙型肝炎病毒的人类免疫缺陷病毒繁殖导致细胞外和细胞内乙型肝炎抗原降低

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摘要

Chronic hepatitis B virus (HBV) infection could cause severe liver disease including cirrhosis, hepatocellular carcinoma, and end-stage liver failure in HIV-positive individuals. The available data from clinical studies suggest that HIV infection modulates the HBV-specific T cell response. However, the virological and molecular aspects of HIV-HBV coinfection are currently poorly understood due to the lack of appropriate model systems. In this study, the effect of HIV infection on the life cycle of HBV was explored using an in vitro model system. The present data show that the extracellular and intracellular hepatitis B surface antigen (HBsAg) and e antigen (HBeAg) decrease significantly in HepG2 cells cotransfected with HIV NL4-3 and pHBV1.3 as compared to those cells transfected only with pHBV1.3. Moreover, a significant decrease in HBV DNA and mRNA expression was also observed in the cotransfected cells. HIV Rev protein, an RNA-bound regulatory protein, could significantly decrease the expression levels of extracellular and intracellular HBsAg and HBeAg by mediating the expression of HBV mRNA in cells cotransfected with plasmids containing HIV-1 Rev and pHBV1.3. Further experiments demonstrate that HIV Rev manipulated neither the promoters of HBV nor the nuclear export of HBV mRNA. These results from the in vitro model system might provide clues to further understand the rapid progression of liver disease in HIV-HBV-coinfected patients.
机译：慢性乙型肝炎病毒（HBV）感染可能导致严重的肝病，包括肝硬化，肝细胞癌和艾滋病毒阳性患者的终末期肝脏衰竭。来自临床研究的可用数据表明HIV感染调节HBV特异性T细胞响应。然而，由于缺乏适当的模型系统，目前艾滋病毒HBV辛凝集的病毒学和分子方面目前很差。在这项研究中，使用体外模型系统探讨了HIV感染对HBV生命周期的影响。本数据表明，与仅用pHBV1.3转染的细胞相比，细胞外和细胞内乙型肝炎表面抗原（HBSAG）和E抗原（HBEAG）在用HIV N14-3和PHBV1.3的细胞中显着降低。此外，在分类细胞中也观察到HBV DNA和mRNA表达的显着降低。通过介导用HIV-1 Rev和PHBV1.3的质粒调解COTRANSFRASFET的细胞中HBV mRNA的表达，HIV REV蛋白（一种RNA含量的调节蛋白）可以显着降低细胞外和细胞内HBsAg和HBeag的表达水平。进一步的实验表明，HIV转申既不操纵HBV的启动子也不是HBV mRNA的核导出。这些来自体外模型系统的结果可以提供以下内容，以进一步了解HIV-HBV-焦收患者肝病的快速进展。

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    Pan Wei; Wu Zuoqiao; Wu Shuwen; Guo Deyin; Gong Xiaoyan; Po Tien;

  • 作者单位

    Wuhan Univ Coll Life Sci Wuhan 430072 Peoples R China;

    Wuhan Univ Coll Life Sci Wuhan 430072 Peoples R China;

    Wuhan Univ Coll Life Sci Wuhan 430072 Peoples R China;

    Wuhan Univ Coll Life Sci Wuhan 430072 Peoples R China;

    Wuhan Univ Coll Chem &

    Mol Sci Wuhan 430072 Peoples R China;

    Wuhan Univ Coll Life Sci Wuhan 430072 Peoples R China;

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  • 正文语种 eng
  • 中图分类 传染病;
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