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West Nile virus, first identified within the United States in 1999, has since spread across the continental states and infected birds, humans and domestic animals, resulting in numerous deaths. Previous studies in mice identified the  Oas1b  gene, a member of the OAS/RNASEL innate immune system, as a determining factor for resistance to West Nile virus (WNV) infection. A recent case-control association study described mutations of human  OAS1  associated with clinical susceptibility to WNV infection. Similar studies in horses, a particularly susceptible species, have been lacking, in part, because of the difficulty in collecting populations sufficiently homogenous in their infection and disease states. The equine  OAS  gene cluster most closely resembles the human cluster, with single copies of  OAS1 ,  OAS3  and  OAS2  in the same orientation. With naturally occurring susceptible and resistant sub-populations to lethal West Nile encephalitis, we undertook a case-control association study to investigate whether, similar to humans ( OAS1 ) and mice ( Oas1b ), equine  OAS1  plays a role in resistance to severe WNV infection. We identified naturally occurring single nucleotide mutations in equine ( Equus caballus )  OAS1  and  RNASEL  genes and, using Fisher's Exact test, we provide evidence that mutations in equine  OAS1  contribute to host susceptibility. Virtually all of the associated  OAS1  polymorphisms were located within the interferon-inducible promoter, suggesting that differences in  OAS1  gene expression may determine the host's ability to resist clinical manifestations associated with WNV infection.

OAS1 Polymorphisms Are Associated with Susceptibility to West Nile Encephalitis in Horses