WNV: Gene Might Figure in Horses' Ability to Fight Virus

Mutations in the gene called OAS1 contribute to a horse's ability to fight West Nile Virus (WNV), reported a group of researchers led by David Adelson, PhD, Professor and Chair of Bioinformatics and Computational Genetics from the University of Adelaide in South Australia.

Previous research in mice indicated that the OAS genes played a role in immunity to flaviviruses (such as WNV). Horses also have OAS genes that produce proteins known to break down viral genetic material.

"Since animals' susceptibility to the West Nile Virus is variable and horses are particularly susceptible to severe infections, this study was conducted to determine if mutations in the OAS genes contribute to a horse's ability to fight off the virus," explained Adelson.

Indeed, OAS1 gene mutations were identified in the 44 horses that succumbed to fatal WNV infection during the initial US epidemic in 2001 and 2002.

"Six different mutations were located in a particular part of the gene called the 'interferon-inducible promoter,' and each of these mutations involved only a single, small change in the gene sequence," said Adelson. "This study suggests that certain OAS1 gene variants may determine a horse's ability to resist clinical manifestations associated with WNV infection."

Adelson was unable to disclose information regarding ongoing studies in this field.

The study, "OAS1 polymorphisms are associated with susceptibility to West Nile encephalitis in horses," was published in the May edition of the online journal PLoS ONE.

About the Author

Stacey Oke, DVM, MSc

Stacey Oke, MSc, DVM, is a practicing veterinarian and freelance medical writer and editor. She is interested in both large and small animals, as well as complementary and alternative medicine. Since 2005, she's worked as a research consultant for nutritional supplement companies, assisted physicians and veterinarians in publishing research articles and textbooks, and written for a number of educational magazines and websites.

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