呼吸道合胞病毒是造成婴幼儿及老年人因下呼吸道疾病死亡的重要病原体。迄今，尚无批准的RSV疫苗和特异性治疗药物，归其原因是RSV感染介导肺损伤机制尚未阐述清楚。前期我们建立RSV感染致病关键因子基因数据库，能够较为全面地描绘其感染过程。从中我们发现核糖体蛋白S6激酶-4（MSK-2）不仅能调控RSV介导的炎症反应，而且促进RSV诱导自噬小体形成。有趣的是，干预RSV诱导自噬增强炎症应答。本课题进一步对MSK-2促自噬分子机制进行探讨，基于自噬抑制炎性因子变化，开展对MSK-2、自噬与炎症反应的内在联系深入探究，提出“MSK-2促进RSV诱导自噬进而调节炎症反应”，即“MSK-2-自噬-炎症”假说，为RSV的科学防控提供理论依据。

Respiratory syncytial virus (RSV) is critical pathogen of severe airway disease casing death in infants and the elder people. To date, There is still no vaccine and limited specific drugs in markets, attributing to the mechanisms of RSV-induced lung injury remaining elusive. Previously, we’ve achieved the database associated with RSV via whole human genome siRNA screening，which described comprehensively the RSV infection. From database, we found that MSK-2 could negatively regulate the inflammatory cytokines, and also promoted the formation of autophagy induced by RSV. Interestingly, if RSV-induced autophagy were intervened by inhibitor 3-MA , the inflammatory cytokines increased significantly. In the project, we would investigate the molecular mechanism of MSK-2-promting autophagy. And we have knew that autophagy played a critical role in inhibiting inflammatory cytokines. This project would figure out the inner link of “MSK-2, autophagy and inflammatory cytokines”Therefore, it hypothesis that” MSK-2-autophagy-inflammatory cytokines”, which provides new idea for the pathogenesis of RSV-induced lung injury. Also the hypothesis could lay a theoretical foundation for the design of rational and effective therapeutic strategy for RSV.