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J Neurovirol. 2019 Aug;25(4):525-539. doi: 10.1007/s13365-019-00752-z. Epub 2019 May 29.

Proteomics analysis of HSV-1-induced alterations in mouse brain microvascular endothelial cells.

Author information

1
Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
2
State Key Laboratory of Virology, CAS Center for Excellence in Brain Science and Intelligence Technology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430000, China.
3
State Key Laboratory of Virology, CAS Center for Excellence in Brain Science and Intelligence Technology, Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan, 430000, China. zhaofei@wh.iov.cn.
4
Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, 410011, China. luwei0338@csu.edu.cn.

Abstract

Herpes simplex virus 1 (HSV-1) is a predominant cause of herpes simplex encephalitis (HSE), leading to a high mortality rate and severe neurological sequelae worldwide. HSE is typically accompanied by the blood-brain barrier (BBB) disruption, but the underlying mechanisms are unclear. To explore the disruption mechanisms of the BBB, quantitative analysis of the cellular proteome was carried out to investigate the proteomic changes that occur after infection. In this study, bEnd.3 cells were infected with HSV-1, followed by liquid chromatography-tandem mass spectrometry. A total of 6761 proteins were identified in three independent mass spectrometry analyses. Compared to the uninfected cells, 386 and 293 differentially expressed proteins were markedly upregulated or downregulated, respectively. Bioinformatic analysis showed that the activator protein-1 factor, including Fos, Jun, and ATF family proteins and cell adhesion molecules were significantly changed. Further validation of the changes observed for these proteins was carried out by western blotting and quantitative real-time PCR. Transendothelial electrical resistance (TEER) studies were performed to explore the effects of ATF3, Fra1, or JunB overexpression on the function of bEnd.3 cells. Characterization of the differential expression of these proteins in bEnd.3 cells will facilitate further exploration of BBB disruption upon HSV-1 infection.

KEYWORDS:

Blood-brain barrier; Herpes simplex encephalitis; Herpes simplex virus 1; Proteome analysis

PMID:
31144288
DOI:
10.1007/s13365-019-00752-z

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