1. Equine arteritis virus does not induce interferon production in equine endothelial cells: identification of nonstructural protein 1 as a main interferon antagonist.
- Author
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Go YY, Li Y, Chen Z, Han M, Yoo D, Fang Y, and Balasuriya UB
- Subjects
- Animals, Arterivirus Infections genetics, Arterivirus Infections immunology, Cricetinae, Endothelial Cells, Equartevirus genetics, Equartevirus immunology, HEK293 Cells, Horses, Humans, Interferon-beta biosynthesis, Interferon-beta genetics, Interferon-beta immunology, RNA, Messenger biosynthesis, RNA, Messenger genetics, RNA, Messenger immunology, Viral Nonstructural Proteins genetics, Arterivirus Infections metabolism, Arterivirus Infections veterinary, Equartevirus metabolism, Immunity, Innate, Interferon-beta antagonists & inhibitors, Viral Nonstructural Proteins metabolism
- 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.
- Published
- 2014
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