HCV以非致细胞病变方式在肝细胞内复制，并逃避细胞固有免疫，这是HCV高发慢性感染的重要原因，认识其机制对于研发抗HCV新药具有重要意义。我们对HCV感染的Huh7细胞进行的转录组测序显示，HCV感染显著上调硫氧还蛋白互作蛋白（TXNIP）的表达；在HCVcc感染的人CD81和occludin转基因（huC/OTg）小鼠，肝组织内TXNIP也显著上调；抑制TXNIP的表达显著降低HCV的复制；I和III型干扰素均能诱导TXNIP的表达。鉴于TXNIP在细胞多种生物途径中的重要调控作用，本课题将以Huh7细胞以及huC/OTg小鼠为模型，以HCV感染诱导的肝细胞氧化应激和内质网应激为切入点，深入探讨TXNIP通过调控细胞自噬、线粒体自噬、非折叠蛋白应答促进HCV复制，保护细胞免于过度应激反应引起的凋亡，以及抑制干扰素的表达与抗病毒活性的可能途径，揭示HCV利用宿主因子实现其持续感染的新机制。

Hepatitis C virus replicates in hepatocytes without causing cytopathic effect, and efficiently escape from the cellular innate immunity, which constitute the major reason for the high incidence of chronic infection of this virus. We found that HCV infection powerfully increased expression of thioredoxin interacting protein (TXNIP) in human hepatocellular carcinoma Huh7 cell line by transcriptome sequencing. In the liver tissue of human CD81 and occludin transgene（huC/OTg）mice infected with HCVcc, TXNIP expression was also greatly elevated. Further analysis showed that knocking-down TXNIP expression by RNA interference greatly reduced HCV replication, and that typeⅠand type Ⅲ interferons induced TXNIP expression. Since TXNIP is an important regulator molecule involving in several biological processes, it is deserved to define the specific function of TXNIP that contribute HCV infection. In this study, Huh7 cells and huC/OTg mice will be used as models for this purpose. From the perspectives of oxidative stress and endoplasmic reticulum stress induced by HCV infection, the mechanisms of TXNIP regulates autophagy, mitophagy and unfolded protein response to enhance HCV replication, protect hepatocytes against apoptosis due to excessive stress responses, inhibit interferons expression and their anti-viral activity will be explored. Hopefully, new strategies that HCV using host factors to achieve its persistent infection would be discovered.