庚型肝炎病毒（GB Virus C,GBV-C）本身不致病，但与HIV共感染可以延缓HIV的疾病进程，GBV-C已经成为治疗HIV的潜在生物治疗剂。然而，在体内GBV-C清除率高，在体外GBV-C感染力差、复制力低，该方面的作用机制目前还没有报道。细胞自噬在宿主抗病毒和清除病毒中发挥着重要作用。据课题组前期研究结果初步显示，细胞自噬具有抵御GBV-C感染的作用。基于此，本研究拟从宿主角度出发，通过对自噬检测实验，验证自噬参与了GBV-C感染细胞的过程；通过诱导和阻断自噬实验，阐明细胞自噬对GBV-C感染的抵御作用；通过时间和剂量依赖实验，找出诱导细胞自噬抵制GBV-C感染的关键蛋白。拟通过该研究，我们期望深入了解细胞自噬抵御GBV-C感染的作用机制，为人类通过调控细胞自噬来诱导GBV-C的感染和复制提供新的思路，为GBV-C更好地应用于HIV患者的治疗提供有效的方法和手段。

GB Virus C/Hepatitis G Virus (GBV-C/HGV) is a positive stranded RNA virus. GBV-C infection has not been associated with any disease. Several studies found that persistent GBV-C infection improved the survival ability in HIV-positive individuals. In fact, GBV-C has been considered as a potential anti-HIV agent. GBV-C has high clearance rate in vivo, low infection power and replication capacity in vitro. However, the mechanisms are not clearly understood. Autophagy played important roles in host antiviral defense. Preliminary data showed that autophagy had protective effects on GBV-C infection. Based on these lines of evidence, the current project will validate that GBV-C induce autophagy through detection of the autophagosome using electron microscope and laser confocal microscope. Further experiments will validate the influence of autophagy on GBV-C replication through induction and inhibition of autophagy. Finally, the interaction between the constitutive protein of GBV-C and autopahgy-related protein will be determined by using Co-IP and confocal assay. We eager to deeper understand the mechanism of autophagy on GBV-C infection and provide theoretical support for clinical treatment for HIV.