Equine herpesvirus-1 suppresses type-I interferon induction in equine endothelial cells.

Abstract

Equine herpesvirus-1 (EHV-1) is one of the most common and important respiratory viral pathogens of horses. EHV-1 in horses replicates initially in the respiratory epithelium and then spreads systematically to endothelial cells lining the small blood vessels in the uterus and spinal cord, and highly pathogenic virus strains can produce aborted fetuses or myeloencephalopathy. Like other herpes viruses, EHV-1 employs a variety of mechanisms for immune evasion. Some herpes viruses down-regulate the type-I interferon (IFN) response to infection, but such activity has not been described for EHV-1. Here, in an in vitro system utilizing an established equine endothelial cell line, we studied the temporal effect on IFN-β responses following infection with the neuropathogenic T953 strain of EHV-1. Results show that after an early induction of IFN-β, the virus actively shut down further production of IFN-β and this was correlated with expression of the viral late genes. Expression of the IFN response factor viperin, a marker of host cell type-I IFN responses, was also suppressed by T953 virus infection. EHV-1-mediated suppression of host type-I IFN responses may play an important role in EHV-1 pathogenesis and the mechanism of this, presumably involving a viral late gene product, warrants investigation.