丙型肝炎病毒（HCV）是1989年首次分离鉴定出来的一种非甲非乙型的肝炎病毒。HCV的高度变异性以及耐药性突变病毒的产生使得单纯依赖目前的药物及治疗方案将难以应。p7是HCV中唯一的离子通道蛋白，实验表明，p7对病毒晚期颗粒的组装和成熟病毒颗粒的释放是必不可少的，突变和完全删除p7会导致病毒不能产生感染性。因此抑制p7离子通道就可以抑制病毒的感染活性，将p7作为一个新的药物靶点进行抗丙肝病毒药物研发。本研究基于p7核磁结构并结合分子动力学确定了HMA的活性位点；通过计算机辅助设计筛选新的化合物结构；利用体外p7脂质体功能实验及HCV病毒细胞实验评估目标化合物抑制能力，期望找到特异性抑制p7离子通道活性的药物先导化合物，为未来治疗丙肝提供新的药物选择。

Hepatitis C virus (HCV) infection is a rising global health problem. The p7 protein is the only viroporin encoded by the HCV genome and has been sought after as a potential anti-HCV drug target. The ion channel activity of p7 can be blocked by several inhibitors, including rimantadine, hexamethylene amiloride (HMA), and long alkylchain iminosugar derivatives. The high variability of HCV is always a potential problem. The depending on the current drug and treatment will be difficult to respond to variations in different genotypes of HCV. This research subject is based on p7 of structure to design new drug molecules or lead compounds combined with structure biology in atomic level mainly using computer aided drug design and the molecular simulation technology. Using NMR technology studies the specific selectivity of p7, the active site of p7-ligand complex and the effect factors of interaction. Combined with site-directed mutagenesis and multiple function test illustrates the relationship between p7 channel activity and biological function as well as the structure-activity relationship between p7 and different inhibitors, and thus open up a new route for new anti-HCV drug development.