Effect of VIM in EV71 infection in human microvascular endothelial cells
10.3969/j.issn.1006-5725.2016.10.003
- VernacularTitle:VIM在肠道病毒71型侵染人脑微血管内皮细胞中的作用
- Author:
Yanyun ZHONG
;
Bao ZHANG
;
Mingliang HE
;
Yujuan CAO
;
Xianbo WU
- Publication Type:Journal Article
- Keywords:
HBMEC;
VIM;
Enterovirus 71;
Receptor
- From:
The Journal of Practical Medicine
2016;32(10):1560-1563
- CountryChina
- Language:Chinese
-
Abstract:
Objectives To study the effect of VIM in Enterovirus 71 (EV71) infection of (human brain microvascular endothelial cells (HBMEC) and elaborating the mechanism of EV71 infection in the nervous system. Methods Knocked out the VIM by CRISPR technology , the differences in EV71 absorption , replication , release between wild VIM and VIM knocked-out (VIM-KO) HBMEC were detected by fluorescence quantitative PCR. Results 4 ℃ absorption experiment conformed that EV71 adsorption in VIM- KO is 40% less than in the normal HBMEC. After EV71 infect HBMEC for 48 h (48 h p. i.), the quantitative PCR result showed intracellular viral RNA in VIM-KO was only 1/12 of that in the normal HBMEC. Also the extracellular viral RNA was quantified, and the number of cells in VIM-KO had been reduced 1.4 times compared with the normal HBMEC. Conclusions Once VIM knocking out, EV71 attachment has been obviously reduced. Meanwhile, the level of viral RNA replication and release are decreased compared with the normal HBMEC. VIM may be an attachment receptor of EV71 in HBMEC , when the virus invades HBMEC with the binding of VIM. Moreover , VIM plays an important role in the replication and release of EV71.