Transcriptional response of human umbilical vein endothelial cell to H9N2 influenza virus infection

被引：8

作者：

Wang, Wei ^{[1
]}

Mu, Xiang ^{[2
]}

Zhao, Lihong ^{[1
]}

Wang, Jianfang ^{[2
]}

Chu, Yaocheng ^{[3
]}

Feng, Xuejian ^{[1
]}

Feng, Bo ^{[1
]}

Wang, Xiaohong ^{[1
]}

Zhang, Jianjun ^{[2
]}

Qiao, Jian ^{[1
]}

机构：

[1] China Agr Univ, Coll Vet Med, Dept Pathophysiol, Beijing 100193, Peoples R China

[2] Beijing Agr Coll, Dept Anim Sci & Technol, Beijing 102206, Peoples R China

[3] Hebei North Univ, Dept Vet Med, Coll Anim Sci, Zhangjiakou 075131, Hebei Province, Peoples R China

来源：

VIROLOGY | 2015年 / 482卷

基金：

中国国家自然科学基金;

关键词：

H9N2; virus; Human umbilical vein endothelial cell; Microarray; Gene expression profile; INTERFERON-STIMULATED GENES; AVIAN H9N2; A VIRUS; RECEPTOR SPECIFICITY; BINDING-SITES; PATHOGENESIS; EXPRESSION; CHEMOKINES; EVOLUTION; APOPTOSIS;

D O I：

10.1016/j.virol.2015.03.037

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

Endothelial cells are believed to play an important role in response to virus infection. Here, we used a microarray technology to study the gene expression profile in human umbilical vein endothelial cells at 24 h postinfection with H9N2 viruses or inactivated H9N2 viral particles. The results showed that H9N2 virus infection induced an abundance of differential expressed genes, exhibiting a transcriptional signature of viral infection. High levels of chemokine gene expressions were detected following treatment. Surprisingly, the most significantly up-regulated genes were mainly interferon-stimulated genes (ISGs), although there was no change in interferon gene expression and interferon protein level. We also found that viral particles were more potent than viruses in inducing ISGs expression. These results suggest that induction of expression of ISGs is mainly dependent on the interaction between viral particles and endothelial cells. Our data offer further insight into the interaction between endothelial cells and H9N2 influenza viruses. (C) 2015 Elsevier Inc. All rights reserved.

引用

页码：117 / 127

页数：11

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