Researchers have identified a genetic vulnerability that makes stallions infected by the equine arteritis virus more likely to become carriers.
The troublesome pathogen, which causes equine viral arteritis, can be detected with a Coggins blood test. The disease rose to global prominence in 1984 during an outbreak in Kentucky. Infected horses have been recorded in many countries.
Clinical signs vary. The typical picture is a fever, upper respiratory tract inflammation and discharges, weakness, depression, anorexia, limb swelling, sheath and scrotal swelling in stallions, and abortion in pregnant mares, usually from two months of gestation onwards. However, many cases present with little more than a loss of appetite.
It can also cause severe respiratory disease and inflammation of the small intestine in young foals.
Severity tends to be greater in old, young or debilitated animals.
Outbreaks result in significant economic losses to the equine industry due to high rates of foal loss in pregnant mares, death in young foals and establishment of the carrier state in stallions. The virus is maintained in the horse population between breeding seasons by persisting in these carrier stallions.
Fresh research at the University of Kentucky’s Maxwell H. Gluck Equine Research Center has shed new light on factors involved in stallions becoming carriers.
Professor Udeni Balasuriya and his colleagues, writing in the peer-reviewed open-access journal PLOS ONE, noted that a variable proportion of infected stallions – 10% to 70% – can become persistently infected and continue to shed the virus in their semen for periods ranging from several months to life.
The study team had recently reported that some stallions possessed a subpopulation of CD3+ T lymphocytes (a form of white blood cell) that were susceptible to the infection under laboratory conditions. The researchers found that the presence of these cells was associated with long-term carrier status following exposure to the virus.
“In contrast, stallions not possessing the CD3+ T lymphocyte susceptible phenotype are at less risk of becoming long-term virus carriers,” they reported.
The study team traced this genetic vulnerability back to equine chromosome 11, and have now gone on to establish that mutations within the CXCL16 were responsibile for this carrier vulnerability.
“Genetic and experimental studies were used to demonstrate that CXCL16 in the horse codes for two proteins, one associated with resistance and the other associated with susceptibility of CD3+ T lymphocytes to EAV infection,” they wrote.
They said although the differences between horses’ susceptibility through their CD3+ T lymphocytes was interesting, it was the association between the CXCL16 genotype and long-term carrier status in stallions that was of major importance because these animals were key to the survival of the virus in horses.
Sarkar S, Bailey E, Go YY, Cook RF, Kalbfleisch T, Eberth J, et al. (2016) Allelic Variation in CXCL16 Determines CD3+ T Lymphocyte Susceptibility to Equine Arteritis Virus Infection and Establishment of Long-Term Carrier State in the Stallion. PLoS Genet 12(12): e1006467. doi:10.1371/journal.pgen.1006467