研究卡波氏肉瘤病毒表达的潜伏相关核抗原（LANA）能否招募SIN3转录调控蛋白家族成员A（Sin3A），以及Sin3A结合的HDAC1/HDAC2的去乙酰化酶活性能否降低KSHV附加体基因组DNA所结合组蛋白的乙酰化修饰水平，最终通过降低潜伏-裂解分子开关ORF50启动子区的转录活性使得KSHV维持潜伏感染；研究LANA招募Sin3A是否与宿主细胞内Mad/Max和Sin3A的之间互作构成竞争关系，以及c-Myc是否因此从转录抑制状态转变成激活状态并增强宿主细胞的增殖活性；尝试敲减低表达KSHV阳性细胞中的LANA，获得以LANA为靶点的抗KSHV及其肿瘤治疗的实验与理论依据。. 以上内容的研究，将发现KSHV维持潜伏感染并促进宿主细胞转化的分子机制，为以LANA作为抗KSHV及其肿瘤治疗的新靶点提供实验与理论依据。

KSHV encoded Latency Associated Nuclear Antigen (LANA) , one abundantly expressed viral protein in latency, has been closely related to the maintenance of KSHV latency. However, the mechanism by which LANA involve in the regulation of KSHV life cycle still remain elusive. Previous study have revealed the important role of histone acetylation in regulating the transcription activity of the key lytic-latency switcher RTA. Here, we focus on the possibility of the recruitment of Sin3A and Sin3A associated HDAC1/HDAC2 by LANA, and the potential effect on the acetylation of histone associated with KSHV episome. . The research will further enrich the pathogenesis of KSHV. Moreover , this work will provide potential new targets for the treatment of KSHV associated malignant.