Serologic Response of Horses to the Structural Proteins of Equine Arteritis Virus

Autor: MacLachlan, N. James, Balasuriya, Udeni B. R., Hedges, Jodi F., Schweidler, Therese M., McCollum, William H., Timoney, Peter J., Hullinger, Pamela J., Patton, John F.
Zdroj: Journal of Veterinary Diagnostic Investigation; July 1998, Vol. 10 Issue: 3 p229-236, 8p
Abstrakt: Equine arteritis virus (EAV) is the causative agent of equine viral arteritis, an apparently emerging disease of equids. In this study, the antibody response of horses to the structural proteins of EAV was evaluated using gradient-purified EAV virions and baculovirus-expressed recombinant EAV structural proteins (GL, GS, M, N) as antigens in a Western immunoblotting assay. Thirty-three sera from horses that previously had been naturally or experimentally infected with EAV were evaluated, including samples from mares, geldings, and both persistently and nonpersistently infected stallions. Sera also were evaluated from 4 horses that had been vaccinated with the commercial modified live EAV vaccine. The data suggest that the serologic response of individual horses to EAV may vary with the infecting virus strain and duration of infection. The M protein was most consistently recognized by the various serum samples, whereas the response to the N and GLproteins was variable and the GSprotein was bound by only 1 serum sample. The immunoblotting assay definitively established the protein specificity of the humoral response of horses to EAV; however, it clearly is less sensitive than the standard serum neutralization (SN) test—2 of the 37 sera that were serpositive by th SN test failed to react in the immunoblot assay with any EAV structural protein. Furthermore, the GLprotein expresses the known neutralization determinants of EAV, yet only 22 of the 37 sera that had SN antibodies bound the GLprotein in the immunoblotting assay. Information from this study will assist ongoing efforts to develop improved methods for the serologic diagnosis of EAV infection of horses.
Databáze: Supplemental Index