Iron metabolism and hepatitis C virus

丙型肝炎病毒（HCV）感染是全球严重的卫生保健问题，是血液传播慢性肝炎、肝硬化和肝细胞癌的主要原因。HCV感染的过程受到多种因素的影响，包括体内的铁状态。在这里，我们将采用HCV复制的细胞培养模型（感染性“复制子”）来研究HCV影响全身和细胞铁稳态的机制。我们最近发现，对HCV感染细胞施用铁可显著降低病毒复制。在早期的实验中，我们也证明了铁抑制HCV RNA聚合酶的功能，这是病毒复制所必需的蛋白质。考虑到铁超载会加重病毒性丙型肝炎，这些发现出乎意料；因此，我们的数据表明，铁对hcv感染患者的不良临床影响是间接的。

Infection with hepatitis C virus (HCV) poses a serious health care problem worldwide and is the leading cause of blood-transmitted chronic hepatitis, liver cirrhosis and hepatocellular cancer. The course of HCV infection is affected by various factors, including the body's iron status. Here we will employ a cell culture model for HCV replication (infectious "replicon") to study mechanisms by which HCV affects systemic and cellular iron homeostasis. We recently showed that administration of iron to HCV infected cells dramatically decreases viral replication. In earlier experiments, we also demonstrated that iron inhibits the function of the HCV RNA polymerase, a protein essential for viral replication. These findings are unexpected, considering that iron overload aggravates viral hepatitis C; thus, our data suggest that the adverse clinical effects of iron on HCV-infected patients are indirect.