Dumoulin Franz Ludwig, von dem Bussche Annette, Li Jisu, Khamzina Leila, Wands Jack R, Sauerbruch Tilman, Spengler Ulrich
Department of Medicine I, University of Bonn, Sigmund Freud Strasse 25, Germany.
Virology. 2003 Jan 20;305(2):260-6. doi: 10.1006/viro.2002.1701.
The mechanisms leading to viral persistence and hepatocarcinogenesis in hepatitis C virus (HCV) infection are not fully understood. Recently, evidence has been accumulated that HCV viral proteins might interfere with gene expression of host cells. Here, we demonstrate that the amino-terminal portion of HCV NS2 protein inhibits the expression of reporter genes driven by different promoters or enhancer elements and also inhibits hepatitis B virus (HBV) gene expression and HBV DNA replication. The inhibitory effect of HCV NS2 on liver and non-liver-specific promoters and enhancer elements might be relevant for the pathogenesis of chronic HCV infection.
丙型肝炎病毒（HCV）感染导致病毒持续存在和肝癌发生的机制尚未完全明确。最近，有证据表明HCV病毒蛋白可能会干扰宿主细胞的基因表达。在此，我们证明HCV NS2蛋白的氨基末端部分可抑制由不同启动子或增强子元件驱动的报告基因的表达，还可抑制乙型肝炎病毒（HBV）的基因表达和HBV DNA复制。HCV NS2对肝脏和非肝脏特异性启动子及增强子元件的抑制作用可能与慢性HCV感染的发病机制有关。
