随着医院疾病谱的改变，一些古老的传染病濒临消灭，然而曾经得到控制的卷土重来。2018年8月流行性乙型脑炎（JE)在宁夏局地暴发流行，部分病人以四肢瘫痪、呼吸肌麻痹为首发，早期易被误诊为格林巴利综合征。致残率和死亡率高，引起短暂的社会恐慌和各级政府的高度重视。国内外仅有1例相关文献报道，但确切发病机制不清。经病毒分离为JEV基因Ⅰ型、外周血液检测抗GM3阳性、腓肠神经活检示轴索损害，推测JEV感染后宿主细胞可能产生如抗GM3抗体等类似蛋白，与周围神经细胞膜结合导致运动神经轴索变性。因此，筛选关键蛋白、探索其发病机制是重点关注的科学问题。本课题基于蛋白组学和单细胞测序技术筛选JE周围神经损害患者外周血液和脑脊液的差异蛋白和功能验证；研究JEV与宿主蛋白的互作机制，探讨关键蛋白与蛋白泛素化修饰和相关信号通路；揭示JE周围神经损害发病机制，为今后JE综合防控提供实验室依据。

As the hospital's disease spectrum changes, some ancient infectious diseases are on the verge of extinction, but once the control has come back. In August 2018, epidemic encephalitis (JE) was prevalent in Ningxia. Some patients started with quadriplegia and respiratory muscle paralysis. They were misdiagnosed as Guillain-Barre syndrome in the early stage. High morbidity and mortality rates cause short-lived social panic and high priority from all levels of government. There is only one relevant literature report at home and abroad, but the exact pathogenesis is unclear. The virus was isolated as JEV gene type I, peripheral blood test anti-GM3 positive, and sural nerve biopsy showed axonal damage. It is speculated that host cells may produce similar proteins such as anti-GM3 antibody after JEV infection, and bind to peripheral nerve cell membrane to cause motor axis denaturation. Therefore, screening key proteins and exploring their pathogenesis are the key scientific issues. This study is based on proteomics and single-cell sequencing technology to screen differential proteins and functional verification of peripheral blood and cerebrospinal fluid in patients with peripheral nerve damage in JE. Study the interaction mechanism between JEV and host proteins, and explore the key protein and protein ubiquitination modification and related signals Pathway; reveals the pathogenesis of nerve damage around JE, and provides laboratory basis for JE comprehensive prevention and control in the future.