Tscherne Donna M, Evans Matthew J, von Hahn Thomas, Jones Christopher T, Stamataki Zania, McKeating Jane A, Lindenbach Brett D, Rice Charles M
Laboratory of Virology and Infectious Diseases, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
J Virol. 2007 Apr;81(8):3693-703. doi: 10.1128/JVI.01748-06. Epub 2007 Feb 7.
Superinfection exclusion is the ability of an established virus infection to interfere with infection by a second virus. In this study, we found that Huh-7.5 cells acutely infected with hepatitis C virus (HCV) genotype 2a (chimeric strain J6/JFH) and cells harboring HCV genotype 1a, 1b, or 2a full-length or subgenomic replicons were resistant to infection with cell culture-produced HCV (HCVcc). Replicon-containing cells became permissive for HCVcc infection after treatment with an HCV-specific protease inhibitor. With the exception of cells harboring a J6/JFH-FLneo replicon, infected or replicon-containing cells were permissive for HCV pseudoparticle (HCVpp) entry, demonstrating a postentry superinfection block downstream of primary translation. The surprising resistance of J6/JFH-FLneo replicon-containing cells to HCVpp infection suggested a defect in virus entry. This block was due to reduced expression of the HCV coreceptor CD81. Further analyses indicated that J6/JFH may be toxic for cells expressing high levels of CD81, thus selecting for a CD81(low) population. CD81 down regulation was not observed in acutely infected cells, suggesting that this may not be a general mechanism of HCV superinfection exclusion. Thus, HCV establishes superinfection exclusion at a postentry step, and this effect is reversible by treatment of infected cells with antiviral compounds.
超感染排除是指已建立的病毒感染干扰第二种病毒感染的能力。在本研究中,我们发现急性感染丙型肝炎病毒(HCV)2a基因型(嵌合株J6/JFH)的Huh-7.5细胞以及携带HCV 1a、1b或2a基因型全长或亚基因组复制子的细胞对细胞培养产生的HCV(HCVcc)感染具有抗性。用HCV特异性蛋白酶抑制剂处理后,含复制子的细胞对HCVcc感染变得敏感。除了携带J6/JFH-FLneo复制子的细胞外,感染的或含复制子的细胞对HCV假颗粒(HCVpp)进入敏感,这表明在初级翻译下游存在进入后超感染阻断。携带J6/JFH-FLneo复制子的细胞对HCVpp感染的惊人抗性提示病毒进入存在缺陷。这种阻断是由于HCV共受体CD81的表达降低。进一步分析表明,J6/JFH可能对高表达CD81的细胞有毒性,从而选择出CD81(低)群体。在急性感染的细胞中未观察到CD81下调,这表明这可能不是HCV超感染排除的普遍机制。因此,HCV在进入后步骤建立超感染排除,并且通过用抗病毒化合物处理感染细胞,这种效应是可逆的。