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Equine arteritis virus does not induce interferon production in equine endothelial cells: identification of nonstructural protein 1 as a main interferon antagonist.

Abstract
The objective of this study was to investigate the effect of equine arteritis virus (EAV) on type I interferon (IFN) production. Equine endothelial cells (EECs) were infected with the virulent Bucyrus strain (VBS) of EAV and expression of IFN-β was measured at mRNA and protein levels by quantitative real-time RT-PCR and IFN bioassay using vesicular stomatitis virus expressing the green fluorescence protein (VSV-GFP), respectively. Quantitative RT-PCR results showed that IFN-β mRNA levels in EECs infected with EAV VBS were not increased compared to those in mock-infected cells. Consistent with quantitative RT-PCR, Sendai virus- (SeV-) induced type I IFN production was inhibited by EAV infection. Using an IFN-β promoter-luciferase reporter assay, we subsequently demonstrated that EAV nsps 1, 2, and 11 had the capability to inhibit type I IFN activation. Of these three nsps, nsp1 exhibited the strongest inhibitory effect. Taken together, these data demonstrate that EAV has the ability to suppress the type I IFN production in EECs and nsp1 may play a critical role to subvert the equine innate immune response.
AuthorsYun Young Go, Yanhua Li, Zhenhai Chen, Mingyuan Han, Dongwan Yoo, Ying Fang, Udeni B R Balasuriya
JournalBioMed research international (Biomed Res Int) Vol. 2014 Pg. 420658 ( 2014) ISSN: 2314-6141 [Electronic] United States
PMID24967365 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • RNA, Messenger
  • Viral Nonstructural Proteins
  • Interferon-beta
Topics
  • Animals
  • Arterivirus Infections (genetics, immunology, metabolism, veterinary)
  • Cricetinae
  • Endothelial Cells
  • Equartevirus (genetics, immunology, metabolism)
  • HEK293 Cells
  • Horses
  • Humans
  • Immunity, Innate
  • Interferon-beta (antagonists & inhibitors, biosynthesis, genetics, immunology)
  • RNA, Messenger (biosynthesis, genetics, immunology)
  • Viral Nonstructural Proteins (genetics, metabolism)

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