Format

Send to

Choose Destination
Virology. 2017 Jul;507:161-169. doi: 10.1016/j.virol.2017.04.023. Epub 2017 Apr 22.

Kobuvirus VP3 protein restricts the IFN-β-triggered signaling pathway by inhibiting STAT2-IRF9 and STAT2-STAT2 complex formation.

Author information

1
State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, PR China.
2
College of Life Sciences, Wuhan University, Wuhan 430072, PR China.
3
College of Life Sciences, Wuhan University, Wuhan 430072, PR China; Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, PR China.
4
State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou 730046, PR China. Electronic address: zhuqiyun@caas.cn.

Abstract

Emerged porcine kobuvirus (PKV) has adversely affected the global swine industry since 2008, but the etiological biology of PKV is unclear. Screening PKV-encoded structural and non-structural proteins with a type I IFN-responsive luciferase reporter showed that PKV VP3 protein inhibited the IFN-β-triggered signaling pathway, resulting in the decrease of VSV-GFP replication. QPCR data showed that IFN-β downstream cytokine genes were suppressed without cell-type specificity as well. The results from biochemical experiments indicated that PKV VP3 associated with STAT2 and IRF9, and interfered with the formation of the STAT2-IRF9 and STAT2-STAT2 complex, impairing nuclear translocation of STAT2 and IRF9. Taken together, these data reveal a new mechanism for immune evasion of PKV.

KEYWORDS:

IFN-β; IRF9; Porcine kobuvirus; STAT2; Signaling pathway; VP3

PMID:
28441586
DOI:
10.1016/j.virol.2017.04.023
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center