Equine viral arteritis (EVA) is a disease of horses caused by an RNA virus of the genus Arterivirus. The virus which causes EVA was first isolated from horses in Ohio in 1953 but the disease has afflicted equine animals worldwide for centuries. It has been more common in some breeds of horses in the United States, but there is no breed “immunity”. In the UK, it is a notifiable disease.There is no known human hazard. The virus which causes EVA is the Equine Arteritis Virus (EAV). Arteriviruses are small, enveloped, animal viruses with an icosahedral core containing a positive-sense RNA genome. The family includes Equine arteritis virus (EAV), porcine reproductive and respiratory syndrome virus (PRRSV), lactate dehydrogenase elevating virus (LDV) of mice and simian haemorrhagic fever virus (SHFV). Infected horses show variable symptoms including fever, depression, oedema, conjunctivitis, abortion and nasal discharge. Some horses show no symtoms of infection (Wiki: Equine viral arteritis).
Vaccine using Venezuelan equine encephalitis replicon particles (VRPs) expressing the two major envelope proteins of EAV as a heterodimer (GL/M) protect horses against subsequent challenge with a virulent strain of EAV. (Balasuriya et al., 2002)
i.
Horse Response
Vaccination Protocol:
EAV-VRPs were diluted in PBS, and six geldings and three mares were each inoculated subcutaneously in the lateral side of the neck with one of the three different EAV-VRPs (pVR21-GL; n=2), M (pVR21-M; n=2) and GL/M (pVR100-GL/M; n=5). Horses were boosted once at 3 weeks after primary immunization by subcutaneous (SC) inoculation with the same EAV-VRP preparation. Two geldings and a mare (control group) were inoculated only with PBS. (Balasuriya et al., 2002)
Immune Response:
Horses immunized with pVR21-GL and pVR21-M VRPs did not develop neutralizing antibodies to EAV, whereas horses immunized with pVR100-GL/M that expresses both the GL and M proteins as a heterodimer developed substantial titers (64–1024) of neutralizing antibodies to EAV (Table 1). The neutralizing antibody titers peaked 2–3 weeks after the booster immunization. Western immunoblotting assay confirmed that horses vaccinated with pVR100-GL/M developed antibodies to both the GL and M proteins of EAV, and that sera from horses vaccinated with the EAV-VRPs that individually express the GL and M proteins weakly recognize the respective immunizing proteins. (Balasuriya et al., 2002)
Side Effects:
All vaccinated horses remained healthy and showed no adverse effects after vaccination. (Balasuriya et al., 2002)
Challenge Protocol:
All horses were challenged with virulent EAV KY84 virus at 5 weeks after booster immunization. Eight horses (geldings) were intranasally challenged with 3.75×10^5 PFU/ml of EAV KY84 that was delivered in 5.0 ml of EMEM using a fenestrated catheter. Estrus was synchronized in four mares by administration of progesterone (Regumate® Hochest-Russel, Germany; 22 mg per horse per day) for 12 days orally) and prostaglandin-F2α (Lutalyse®, Pharmacia and Upjohn, MI; 5 mg per horse, single SC injection), and the mares were challenged during estrus by intrauterine administration of 3.75×105 PFU/ml of EAV KY84 in 5.0 ml of EMEM using an insemination catheter. (Balasuriya et al., 2002)
Efficacy:
The horses that were immunized with pVR21-GL, pVR21-M VRP’s or PBS all developed severe clinical signs of EVA after intranasal or intrauterine challenge with EAV KY84. Two geldings (CZ7947 and KK7999) that were vaccinated with pVR100-GL/M developed no signs of EVA following intranasal challenge with EAV KY84, and the three mares immunized with this replicon construct developed only mild and transient edema around the fetlock joints at 5, 7 and 9 DPI following intrauterine challenge. (Balasuriya et al., 2002)
IV. References
1. Balasuriya et al., 2002: Balasuriya UB, Heidner HW, Davis NL, Wagner HM, Hullinger PJ, Hedges JF, Williams JC, Johnston RE, David Wilson W, Liu IK, James MacLachlan N. Alphavirus replicon particles expressing the two major envelope proteins of equine arteritis virus induce high level protection against challenge with virulent virus in vaccinated horses. Vaccine. 2002; 20(11-12); 1609-1617. [PubMed: 11858869].
2. Balasuriya et al., 2004: Balasuriya UB, Dobbe JC, Heidner HW, Smalley VL, Navarrette A, Snijder EJ, MacLachlan NJ. Characterization of the neutralization determinants of equine arteritis virus using recombinant chimeric viruses and site-specific mutagenesis of an infectious cDNA clone. Virology. 2004; 321(2); 235-246. [PubMed: 15051384].
3. Hedges et al., 1998: Hedges JF, Balasuriya UB, Ahmad S, Timoney PJ, McCollum WH, Yilma T, MacLachlan NJ. Detection of antibodies to equine arteritis virus by enzyme linked immunosorbant assays utilizing G(L), M and N proteins expressed from recombinant baculoviruses. Journal of virological methods. 1998; 76(1-2); 127-137. [PubMed: 9923747].