Label-free proteomics-based analysis of peripheral nerve injury induced by Japanese encephalitis virus

日本脑炎 脑炎 病毒 周围神经 蛋白质组学 病毒学 医学 外围设备 生物 病理 内科学 解剖 基因 生物化学
作者
Xiaoli Wang,Huan Yang,Zhao Wang,Guowei Wang,Liping Yang,Yanping Yuan,Xiaocong Li,Denger Zhang,Kaichun Shen,Zhenhai Wang
出处
期刊:Journal of Proteomics [Elsevier]
卷期号:264: 104619-104619 被引量:3
标识
DOI:10.1016/j.jprot.2022.104619
摘要

Japanese encephalitis (JE) is just an acute encephalitis syndrome contributed to Japanese encephalitis virus (JEV) infection. It the chief causes of viral encephalitis in Asia. In recent years, association of JEV infection with neurological problems such as Guillain-Barré syndrome(GBS) had reported. Nevertheless, its potential pathogenic mechanism has not previously been reported. Therefore, it is urgent to study the relationship between peripheral nerve injury (PNI) and JEV infection. Here, we use the liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique to make out the protein expression levels of mice sciatic nerve between JEV infection group and the sham group. In general, 4303 proteins were designated by MS, and 187 differentially expressed proteins(DEPs) were found. There were 105 proteins up-regulated in the injured sciatic nerve, and 82 proteins were down-regulated. Functional enrichment analysis of DEPs showed that the up-regulated proteins were mainly related to immune regulatory response, and down-regulated proteins were related to ribosomal structural components and translation. SIGNIFICANCE: The Japanese encephalitis virus, a member of the flavivirus, is a Mosquito borne virus. It leads to central nervous system injury by the immune response and inflammation in the brain. In addition, the virus also gave rise to PNI. It is a major public health problem in Asia. The diversity of clinical symptoms has brought serious challenges to the diagnosis and treatment of the disease. Label-Free Proteomics was undertaken to explore the potential mechanisms between JEV and peripheral nervous system in this study. It provided strong evidence that tissue damage is caused by the immune-mediated mechanisms rather than the virus, which offers a basis for the prevention of the disease and further looking for treatment targets.
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