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Engagement of soluble resistance-related calcium binding protein (sorcin) with foot-and-mouth disease virus (FMDV) VP1 inhibits type I interferon response in cells

文献类型： 外文期刊

作者： Li, Xiaying 1 ; Wang, Jianchang 1 ; Liu, Jue 4 ; Li, Zhonghua 1 ; Wang, Yongqiang 1 ; Xue, Yanfei 1 ; Li, Xiaoqi 1 ; Cao, 1 ;

作者机构： 1.China Agr Univ, State Key Lab Agrobiotechnol, Beijing 100193, Peoples R China

2.China Agr Univ, Minist Agr, Key Lab Anim Epidemiol & Zoonosis, Beijing 100193, Peoples R China

3.China Agr Univ, Coll Vet Med, Beijing 100193, Peoples R China

4.Beijing Acad Agr & Forestry, Inst Vet & Anim Sci, Beijing 100097, Peoples R China

关键词： FMDV VP1; Sorcin; Interferon; Immunosuppression

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2013 年 166 卷 1-2 期

页码：

收录情况： SCI

摘要： Foot-and-mouth disease (FMD) is an acute, highly contagious animal disease caused by FMD virus (FMDV). Although FMDV-induced immunosuppression in host has been well established, the exact molecular mechanism for such induction is not very clear. We report here the identification of FMDV VP1 as an interferon-suppressor by interacting with soluble resistance-related calcium binding protein (sorcin). We found that VP1 suppressed tumor necrosis factor (TNF)-alpha or Sendai virus (SeV)-induced type I interferon response in HEK293T cells, and that this suppression could be completely abolished by knockdown of sorcin by shRNA. Furthermore, overexpression of sorcin inhibited type I interferon response. Conversely, TNF- or SeV-induced type I interferon response increased when sorcin knocked down, leading to inhibition of vesicular stomatitis virus (VSV) replication. Thus, VP1-induced suppression of type I interferon is mediated by interacting with sorcin, a protein that appears to regulate cell response to viral infections. (C) 2013 Elsevier B.V. All rights reserved.

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