EB病毒潜伏存在于多数国人体内，但多不致病。条件合适时，潜伏的 EB病毒可重活化，诱导细胞恶性转化，引发淋巴癌、鼻咽癌、胃癌等多种恶性肿瘤。潜伏膜蛋白LMP1和LMP2与EB病毒潜伏态细胞的恶性转化及肿瘤发生相关。LMP1是EB病毒癌基因，其表达产物可劫持肿瘤坏死因子受体CD40介导的信号通路，抑制细胞凋亡和细胞周期调控，诱导细胞癌化。LMP1三聚体化是其活性所需，抑制其寡聚化已成为针对LMP1的药物研发的重要方向。LMP2与LMP1起协同作用，但不直接诱导细胞转化；它可作为信号调节子促进病毒潜伏感染态的建立和维持，阻止EB病毒进入病毒增殖期。LMP2还是我国EB病毒肿瘤免疫治疗疫苗研发的重要靶点。目前尚无LMP1和LMP2三维结构被报道。解析整合膜蛋白LMP1和LMP2的晶体结构，有利于阐明其干预细胞信号的精确分子机理，促进相关药物和疫苗研发，亦代表结构生物学领域国际前沿水平。

Most Chinese individuals are latently and asymptomatically infected with Epstein-Barr virus (EBV). The latent virus can be reactivated, under appropriate conditions, to induce cell malignant transformation and cause many neoplasia, such as nasopharyngeal carcinoma, lymphoma and gastric carcinoma. Latent membrane protein (LMP) 1 and 2 are closely related to the malignant transformation and tumorigenesis of EBV-latently infected cells. LMP1 is an oncogene of Epstein-Barr virus, and the gene-encoded LMP1 protein can hijack CD40-mediated signaling pathway,inhibit apoptosis and cell cycle regulation, and induce cell carcinogenesis. Trimerization of LMP1 is indispensable for its acitivity, and to inhibit LMP1 oligomerization has become a promising drug discovery approach targeting LMP1. LMP2 does not directly induce cell transformation, but play an auxiliary role to LMP1 during tumorgensis. As a signal modulator, LMP2 helps to establish and maintain viral latency, and prevents the reactivation of lytic replication of EB virus. LMP2 is also a considerable vaccine target for immunotherapy of the EBV-associated tumors in China. Currently, no work has been reported on the structure of latent membrane protein 1 or 2. To solve the crystal structures of intramembrane protein LMP1 and LMP2 will be helpful to clarify the molecular mechanism of interference with cell signaling by LMP proteins, and benefit the development of the related drug and vaccine. On the other hand, the project itself presents the world frontier level in structural biology field.