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李建蓉, 王晶, 田昆仑, 王一心, 郭利军, 张雷, 黄汉菊. 静脉药瘾者HIV重叠HBV/HCV感染研究[J]. 中国公共卫生, 2006, 22(5): 513-515. DOI: 10.11847/zgggws2006-22-05-01
引用本文: 李建蓉, 王晶, 田昆仑, 王一心, 郭利军, 张雷, 黄汉菊. 静脉药瘾者HIV重叠HBV/HCV感染研究[J]. 中国公共卫生, 2006, 22(5): 513-515. DOI: 10.11847/zgggws2006-22-05-01
LI Jianrong, WANG Jing, TIAN Kunlun, . Study on co-infection of HIV and HBV/HCV in intravenous drug users[J]. Chinese Journal of Public Health, 2006, 22(5): 513-515. DOI: 10.11847/zgggws2006-22-05-01
Citation: LI Jianrong, WANG Jing, TIAN Kunlun, . Study on co-infection of HIV and HBV/HCV in intravenous drug users[J]. Chinese Journal of Public Health, 2006, 22(5): 513-515. DOI: 10.11847/zgggws2006-22-05-01

静脉药瘾者HIV重叠HBV/HCV感染研究

Study on co-infection of HIV and HBV/HCV in intravenous drug users

  • 摘要:
      目的   探讨人类免疫缺陷病毒(HIV)重叠乙型肝炎病毒(HBV)/丙型肝炎病毒(HCV)感染时, HIV对机体T辅助细胞亚群的影响及HBV/HCV核酸载量的变化。
      方法   以静脉药瘾者(IVDUs)为研究对象, 采用ELISA、免疫层析法和PCR法检测病毒感染指标, 用ELISA法和间接免疫荧光法检测T细胞亚群。
      结果   IVDUs的CD3、CD4细胞、干扰素(IFN)-γ和白细胞介素(IL)-4产生减少, IVDUs存在HIV感染时CD3、CD4细胞和IFN-γ产生进一步降低, HIV感染与HBV-DNA和HBeAg表达相关。
      结论   IVDUsT细胞亚群功能减弱, HIV促进HBV复制, 重叠感染可进一步干扰辅助性T细胞(TH)1/T2细胞平衡, 降低机体细胞免疫功能。

     

    Abstract:
      Objective   To understand T lymphocyte subsets and HBV-DNA/HCV-RNA load with co-infection of HIV and HBV/HCV.
      Methods   A total of 410 Intravenous Drug Users(IVDUs)were recruited with informed consent.Peripheral blood mononuclear cells and sera were separated routinely.Viral markers were detected by ELISA and immunochro-matographic tests.The load of HBV-DNA/HCV-RNA was identified by fluor escence quantitative PCR.The level of PHA-induced IFN-γ/IL-4 was determined by EL ISA.T lymphocyte subset was deter mined by fluorescence immunoassay.
      Results   The level of IFN-γ/IL-4 and the percent of CD3/CD4 cells in IVDUs were lower than that in the healthy controls(P < 0.01).The level of IFN-γ and the percent of CD4 cells were continuously decreased, when the IVDUs was infected with HIV.HBeAg and the load of HBV-DNA were related to HIV-infected.
      Conclusion   Impaired TH response in IVDUs.Virus-infection continuously altered the TH1/TH2 balance.HIV-infection promotes HBV replication.

     

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