现有的临床研究表明，EV71感染所致的手足口病（HFMD）重症及死亡病例的病理特征是中枢神经系统（CNS）的炎症反应和由此引起神经源性肺水肿和/或心肺功能衰竭，而后者作为临床表症的病理生理机制是基于病毒感染而导致的神经内分泌系统失控，我们的前期工作提示，EV71进入CNS后的感染动力学过程很可能与星状胶质细胞这个联系神经系统功能和免疫反应的关键环节相关。因此，本研究拟利用EV71的体外组织培养系统及动物模型系统，主要探索EV71在感染CNS过程中，病毒在星状胶质细胞中增殖导致的星状胶质细胞生物学性状的变化的规律，及其所引起的，CNS中免疫反应与神经内分泌系统相互作用的生物学特征，并确定这一相互作用是否是导致CNS中下丘脑-垂体-肾上腺轴自主性神经系统（ANS）功能失控的病理机制，及其引起心肺系统出现相应功能紊乱临床表现的原因。

The recent clinical study of human hand-foot-mouth disease (HFMD) induced by EV71 infection indicated that the pathogenesis of HFMD severe/death cases induced by EV71 infection presented the brainstem-encephalitis of viral infection followed by pulmonary edema/cardiofailure. The pathophysiological role of later was confirmed as a chaotic process of neuroendocrine in central nerves system (CNS) induced by viral infection, which is related to hypothalamic-pituitary-adrenal axis. Our previous work suggested that the dynamic process of EV71 infection in CNS based on its proliferation in astrocytes, a key component to regulate neuron function and to perform immune response in CNS. In this case, this reasearch, based upon culture system and animal models of EV71 infection established in our lab, will investigate the biological role of astrocytes infected by EV71 and its impact through modified cytokine profile to neuroendocrine. The work in this study also focus on the interaction between immune response performed by infected astrocyte and neuroendocrine, and the biological effect of this interaction in CNS to hypothalamic-pituitary-adrenal axis. This work wish to trace a possible pathogenesis of EV71 infection in CNS and its followed pulmonary edema/cardiofailure presented in clinical process.