State Key Laboratory of Virology, College of Life Sciences, and Chinese-French Liver Disease Research Institute at Zhongnan Hospital, Wuhan University, Wuhan 430072, PR China.
BMC Immunol. 2012 Apr 3;13:15. doi: 10.1186/1471-2172-13-15.
Co-infection with human immunodeficiency virus-1 (HIV-1) and hepatitis C virus (HCV) is associated with faster progression of liver disease and an increase in HCV persistence. However, the mechanism by which HIV-1 accelerates the progression of HCV liver disease remains unknown.
HIV-1/HCV co-infection is associated with increased expression of interferon gamma-induced protein-10 (IP-10) mRNA in peripheral blood mononuclear cells (PBMCs). HCV RNA levels were higher in PBMCs of patients with HIV-1/HCV co-infection than in patients with HCV mono-infection. HIV-1 Tat and IP-10 activated HCV replication in a time-dependent manner, and HIV-1 Tat induced IP-10 production. In addition, the effect of HIV-1 Tat on HCV replication was blocked by anti-IP-10 monoclonal antibody, demonstrating that the effect of HIV-1 Tat on HCV replication depends on IP-10. Taken together, these results suggest that HIV-1 Tat protein activates HCV replication by upregulating IP-10 production.
HIV-1/HCV co-infection is associated with increased expression of IP-10 mRNA and replication of HCV RNA. Furthermore, both HIV-1 Tat and IP-10 activate HCV replication. HIV-1 Tat activates HCV replication by upregulating IP-10 production. These results expand our understanding of HIV-1 in HCV replication and the mechanism involved in the regulation of HCV replication mediated by HIV-1 during co-infection.
人类免疫缺陷病毒 1（HIV-1）和丙型肝炎病毒（HCV）的合并感染与肝脏疾病的更快进展和 HCV 持续存在的增加有关。然而，HIV-1 加速 HCV 肝病进展的机制尚不清楚。
HIV-1/HCV 合并感染与外周血单个核细胞（PBMCs）中干扰素 γ 诱导蛋白-10（IP-10）mRNA 的表达增加有关。HIV-1/HCV 合并感染患者的 PBMCs 中 HCV RNA 水平高于 HCV 单感染患者。HIV-1 Tat 和 IP-10 以时间依赖的方式激活 HCV 复制，HIV-1 Tat 诱导 IP-10 产生。此外，抗 IP-10 单克隆抗体阻断了 HIV-1 Tat 对 HCV 复制的影响，表明 HIV-1 Tat 对 HCV 复制的影响依赖于 IP-10。综上所述，这些结果表明 HIV-1 Tat 蛋白通过上调 IP-10 产生来激活 HCV 复制。
HIV-1/HCV 合并感染与 IP-10 mRNA 的表达增加和 HCV RNA 的复制有关。此外，HIV-1 Tat 和 IP-10 均可激活 HCV 复制。HIV-1 Tat 通过上调 IP-10 产生来激活 HCV 复制。这些结果扩展了我们对 HIV-1 在 HCV 复制中的作用以及 HIV-1 介导的合并感染中调节 HCV 复制的机制的理解。
