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

被引:50
作者
Li, Xiaying [1 ,2 ,3 ]
Wang, Jianchang [1 ,2 ,3 ]
Liu, Jue [4 ]
Li, Zhonghua [1 ,2 ,3 ]
Wang, Yongqiang [1 ,2 ,3 ]
Xue, Yanfei [1 ,2 ,3 ]
Li, Xiaoqi [1 ,2 ,3 ]
Cao, Hong [1 ,2 ,3 ]
Zheng, Shijun J. [1 ,2 ,3 ,4 ]
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
基金
中国国家自然科学基金;
关键词
FMDV VP1; Sorcin; Interferon; Immunosuppression; NF-KAPPA-B; INTEGRIN ALPHA(V)BETA(3); LEADER PROTEINASE; IDENTIFICATION; INFECTION; ALPHA; SWINE; RNA; ACTIVATION; PROTECTION;
D O I
10.1016/j.vetmic.2013.04.028
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
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.
引用
收藏
页码:35 / 46
页数:12
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