Equine viral arteritis: A respiratory and reproductive disease of significant economic importance to the equine industry

Abstract

Summary Equine arteritis virus is the causative agent of equine viral arteritis, a respiratory and reproductive disease that affects the members of the family Equidae. The virus was first isolated from the lung of an aborted fetus after an extensive outbreak of respiratory disease and abortion on a Standardbred breeding farm near Bucyrus, Ohio, in 1953. Since then, periodic outbreaks of equine viral arteritis have been reported in a number of countries around the world. This disease may result in significant economic loss to the equine industry due to the occurrence of abortion in pregnant mares, neonatal mortality, and establishment of the carrier state in stallions. This article provides an extensive review on equine arteritis virus, epidemiology, disease, pathogenesis, and prevention and control measures.

Equine Arteritis Virus Has Specific Tropism for Stromal Cells and CD8+T and CD21+B Lymphocytes but Not for Glandular Epithelium at the Primary Site of Persistent Infection in the Stallion Reproductive Tract

“…KEYWORDS arterivirus, equine arteritis virus, EAV, equine viral arteritis, EVA, persistent infection, male reproductive tract, immunohistochemistry, cellular tropism, immune response E quine arteritis virus (EAV), the prototype member of the family Arteriviridae, genus Arterivirus, in the order Nidovirales (1), is the causative agent of equine viral arteritis (EVA), a respiratory, systemic, and reproductive disease of equids. EAV has a worldwide distribution, and it causes significant economic loss to the equine industry in the United States and other countries (2)(3)(4)(5)(6)(7)(8). EAV contains a positive-sense, single-stranded RNA genome (ϳ12.7 kb) containing 10 known open reading frames (ORFs) (2,3,9,10).…”

“…Acutely infected horses may develop a wide range of clinical signs (influenza-like syndrome), with dependent edema, conjunctivitis, periorbital or supraorbital edema, respiratory distress, urticaria, and leukopenia (2-4, 8, 15, 17-23). However, a remarkable property of EAV is that following initial exposure, it can establish persistent infection in the reproductive tract of stallions, resulting in continuous shedding of infectious virus in semen (2)(3)(4). Although in some cases this ceases at only a few weeks or a few months postinfection, in 10 to 70% of infected stallions shedding can continue for many years or even the remainder of the animal's lifetime (2-4, 18, 24-27).…”

Equine Arteritis Virus Elicits a Mucosal Antibody Response in the Reproductive Tract of Persistently Infected Stallions

“…The strategy employed by EAV to successfully evade host immune surveillance has yet to be determined. Since the carrier stallion plays a pivotal role in the epidemiology of EAV and constitutes the main challenge for its control and potential eradication (1,5,11,12,20), it is important to fully understand the underlying mechanisms involved in the establishment and maintenance of persistent infection in the stallion reproductive tract. Here, we investigated the antibody responses in short-and long-term persistently infected stallions following experimental EAV infection with a specific emphasis on the mucosal antibody response to aid in the understanding of the host immune factors involved in EAV persistence.…”

“…abortion in pregnant mares, and fatal bronchointerstitial pneumonia or pneumoenteric syndrome in foals (12). Most importantly, EAV can establish persistent infection in the reproductive tract of 10 to 70% of infected stallions (carrier state) (13)(14)(15)(16)(17)(18).…”

“…Recently, it has been demonstrated that host genetics are implicated in the outcome of infection (i.e., the short-or long-term carrier state) in the stallion (22,23). Carrier stallions constitute the natural reservoir for EAV and, thus, play a key epidemiological role, as they ensure the maintenance and perpetuation of the virus in equine populations between breeding seasons (1,11,12). Moreover, they constitute a source of viral genetic and antigenic variability that can lead to the emergence of novel variants of the virus (19,(24)(25)(26)(27); B. Nam, Z. Mekuria, M. Carossino, G. Li, Y. Zheng, J. Zhang, R. F. Cook, J. R. Campos, K. M. Shuck, E. Bailey, P. J. Timoney, and U.…”