乙型肝炎严重危害人类健康，但其发病机理尚未完全阐明，尤其是其起源："乙肝病毒（HBV）感染细胞"的具体过程与机制均不明确。本项目在本课题组前期关于慢性乙肝的"遗传机制"与"差异蛋白组学"的研究基础上，继续深入研究"肝脏跨膜蛋白TMEM2"在HBV感染细胞过程中的作用及其机制。本项目使用"慢病毒转染及过表达"、"基因干扰"、"免疫共沉淀"等成熟技术，首先调节TMEM2在细胞中的表达后比较HBV感染状态的变化以明确其与HBV感染的关系，接着研究TMEM2与钠离子-牛磺胆酸共转运多肽（NTCP，最新研究成果证明其为HBV感染的功能性受体）可能存在的竞争或拮抗关系，最后探索它们与NF-kappaB信号转导系统在HBV感染过程中的作用及相互影响，并试图最终阐明TMEM2在HBV感染细胞过程中的机制，为最终明确HBV感染机制提供研究基础和新的研究途径。

Hepatitis B do serious harm to human health without pathogenesis been clarified, especially the source of chronic hepatitis B: process and mechanism of HBV infection into cells. This research is to discover the effects and mechanism of TMEM2 in the HBV infection into cells, based on our previous study about the genetic mechanism and differential proteomics of HBV infection. Some well-handling techniques were used in this research including lentivirus transfection, gene over-express, gene interfering, co-immunoprecipitation and so on. We want to investigate the effects on the HBV infection ability caused by TMEM2 expression changes in the cells, the competition or antagonism relationship between TMEM2 and NTCP, their effects and influences in the NF-kappaB signal transduction system in HBV infection process. We hope that the role and mechanism of TMEM2 in HBV infection on cells could be revealed, which can provide basis and new strategy to the research of HBV infection mechanism.