课题组前期发现负性分子CD244的高表达与HBV持续感染有关，调控CD244的关键分子可能成为HBV感染慢性化的新标志物。结合最新研究和前期试验推测miR-330-3p可能通过结合靶基因CD244介导HBV免疫逃逸。根据最新热点：lncRNA可作为ceRNA竞争性结合microRNA影响疾病进展，课题组通过生物信息学预测、lncRNA芯片及定量，推测lnc-AIFM2-1竞争性结合miR-330-3p，减弱后者对CD244的抑制，介导CTLs功能耗竭及HBV免疫逃逸。课题组拟分析慢性HBV感染者及自发清除者lnc-AIFM2-1、miR-330-3p及CD244的表达，并用siRNA等技术在细胞和小鼠模型验证。预期将揭示，lnc-AIFM2-1作为ceRNA介导miR-330-3p调控CD244表达，介导HBV感染慢性化，对研究表观修饰在HBV免疫逃逸中的作用和探寻新靶标具有重要意义。

Previous results of our group indicated over-expression of coinhibitory molecule CD244 was associated with HBV persistence, but the mechanism was unclear. miR-330-3p was reported to target CD244, thus induce CTLs function exhaustion and HBV immune escape. Newly studies reported lncRNA can act as ceRNA, interact with microRNA, mediated disease progress. Our bioinformatics predict and chip screening results indicated lnc-AIFM2-1 was significantly higher in chronic HBV infected patients, and it can target to miR-330-3p. We speculate Lnc-AIFM2-1 contributes to over-expression of CD244 by acting as a ceRNA against miR-330-3p in HBV immune escape. This study aims to find new biomarkers for HBV infection by kinds of molecular biological techniques such as RT-PCR、siRNA、Western blot and so on.