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.

Highlights

  • Equine arteritis virus (EAV) is the causative agent of equine viral arteritis, a respiratory and reproductive disease of horses [1, 2]

  • Sendai virus- (SeV-)induced IFN-β mRNA expression, at both 3 and 6 hpi, was significantly suppressed in cells previously infected with EAV

  • vesicular stomatitis virus (VSV)-GFP replication was not inhibited in MDBK cells that were preincubated with cell culture supernatant from endothelial cells (EECs) infected with EAV alone

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Summary

Introduction

Equine arteritis virus (EAV) is the causative agent of equine viral arteritis, a respiratory and reproductive disease of horses [1, 2]. EAV is a small enveloped virus with a positive-sense, single-stranded RNA genome of ∼12.7 kb. It belongs to the family Arteriviridae (genus Arterivirus, order Nidovirales), which includes porcine reproductive and respiratory syndrome virus (PRRSV), simian hemorrhagic fever virus (SHFV), and lactate dehydrogenase-elevating virus (LDV) of mice [3,4,5]. The remaining eight ORFs (2a, 2b, and 3, 4, 5a, 5b, and 6-7) are located in the 3󸀠 quarter of the genome and encode the structural proteins (E, GP2, GP3, GP4, ORF5a protein, GP5, M, and N, resp.) of the virus [5, 6, 11,12,13]

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