呼吸道合胞病毒（RSV）是引起婴幼儿呼吸道感染最常见和最重要的病毒病原，生命早期重症RSV感染与学龄期反复喘息密切相关，是儿童哮喘发生的独立危险因素。课题组前期研究发现RSV感染后期Th2类细胞因子显著升高，并介导了慢性气道炎症和气道高反应性（AHR）。在此基础上，本项目拟建立不同免疫背景小鼠RSV感染模型，采用流式细胞术、体外原代细胞培养、慢病毒体内转染等方法系统研究RSV感染后期Th2类细胞因子的来源、始动机制与相关信号通路，明确非特异性过敏原刺激或病原感染是否导致RSV感染后期建立的Th2类免疫应答持续存在或过度增强，最终导致慢性气道炎症和AHR。研究结果将进一步揭示RSV感染引起反复喘息/哮喘发生的机制，为临床寻找防治病毒感染后所致慢性气道炎症性疾病新靶点提供充分的理论依据。

RSV (Respiratory Syncytial Virus) is the primary cause of respiratory tract infections among infants worldwide. Severe RSV infection early in life has been intimately associated with subsequent recurrent wheezing in school age children and also acts as an independent risk factor for the development of childhood asthma. However, the underlying mechanisms are largely unknown. We have demonstrated that during the later phase of RSV infection, being consistent with asthma, Th2-like cytokines robustly increased and accounted for chronic airway inflammation ahd airway hyperresponsiveness (AHR). Here in the recent research, methods as flow cytometry, primary culture and lentiviral transfection are used in several mouse models to determine the cellular sources, the initiating factors as well as the potential signaling pathways of RSV-associated Th2-like cytokines. Further studies are programmed to define that the relatively harmless non-specific stimuli and microorganism infection can boost or sustain RSV-induced Th2-like immune responses and ultimately result in the development of chronic airway inflammation and AHR.Such work will help to shed new light on the underlying mechanisms of recurrent wheezing and asthma after early life RSV infection and thus might lead to new promissing therapeutic strategies for chronic airway diseases.