Identification of Genetic Factors Responsible for Establishment of Equine Arteritis Virus Carrier State in Stallions.

Outbreaks of equine viral arteritis (EVA) result in significant economic losses to the equine industry due to high rates of abortion in pregnant mares, death in young foals, and establishment of the carrier state in stallions. Recently, we demonstrated an association between establishment of the long-term equine arteritis virus (EAV) carrier status in stallions and in vitro susceptibility of a CD3+ T cell subpopulation to EAV infection. A genome wide association study (GWAS) has shown that CD3+ T cell susceptibility is associated with a dominant haplotype on equine chromosome 11 (ECA11) in different horse breeds. Therefore, we hypothesize that CD3+ T cell susceptibility to EAV infection and establishment of persistent infection in stallions have common mechanisms of genetic control. To test this hypothesis, the focus of the proposed studies is to: (i). identify genetic differences on ECA11 using targeted re-sequencing and conduct a more powerful GWAS analysis to determine if involvement from additional genomic locations can be identified; (ii). identify the EAV susceptible CD3+ T cell subpopulation and compare its mRNA transcriptome to that of EAV resistant CD3+T-cells; (iii). identify the EAV cellular entry receptor and its relationship with ECA11; and (iv). conduct experimental infection of stallions to define the relationships between genotype, cellular pathology, and EAV persistence (research). The studies provide research training opportunities for graduate and undergraduate students to address an important infectious disease problem through integrating functional genomics and proteomics (education). Findings from these studies wil