EQUINE VETERINARY EDUCATION Equine vet. Educ. (2018) 30 (9) 497-512 doi: 10.1111/eve.12672


Review Article


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


U. B. R. Balasuriya*, M. Carossino and P. J. Timoney Department of Veterinary Science, Maxwell H. Gluck Equine Research Center, College of Agriculture, Food and Environment, University of Kentucky, Lexington, USA. *Corresponding author email: ubalasuriya@uky.edu


Keywords: horse; equine arteritis virus; equine viral arteritis; arteritis; abortion; carrier stallion; international trade


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.


Introduction


Equine viral arteritis (EVA) is a well-known reproductive and respiratory disease of horses and other equids caused by equine arteritis virus (EAV) (Doll et al. 1957a; McCollum et al. 1971; Cole et al. 1986; Timoney and McCollum 1987; Glaser et al. 1996, 1997; Cavanagh 1997; MacLachlan and Balasuriya 2006; Balasuriya and MacLachlan 2013; Balasuriya et al. 2013). Although the vast majority of EAV infections are subclinical, outbreaks of the disease do occur and are most importantly associated with abortion, neonatal mortality and establishment of persistent infection in stallions (Doll et al. 1957a,b; Cole et al. 1986; Timoney et al. 1986; Vaala et al. 1992; Del Piero et al. 1997; Balasuriya et al. 1999a; Hedges et al. 1999; Timoney and McCollum 2000). Persistently infected stallions play a central role in the maintenance, perpetuation, and evolution of the virus in the horse population. An increase in the incidence of the disease has been observed in the past 20 years, associated inter alia with increased national and international movement of horses and shipment of frozen or chilled semen (McCollum et al. 1998; Balasuriya et al. 1999a; Hedges et al. 1999; Timoney 2000a,b; Guthrie et al. 2003; Zhang et al. 2007, 2010a; Olguin Perglione et al. 2010; Broaddus et al. 2011a; Miszczak et al. 2012). This review article provides an update of the advances on the causative agent (EAV), disease (EVA), pathogenesis, establishment and maintenance of the carrier state, and proper implementation of control and prevention measures to prevent disease outbreaks.


Equine arteritis virus


Equine arteritis virus is an enveloped, positive-sense, single- stranded RNA virus that is considered to be the prototype


member of the family Arteriviridae, genus Arterivirus (order Nidovirales), a taxonomic grouping that includes porcine reproductive and respiratory syndrome virus, simian haemorrhagic fever virus, lactate dehydrogenase-elevating virus of mice, and the recently identified wobbly possum disease virus of free-ranging Australian brushtail possums (Trichosurus vulpecula) in New Zealand (Cavanagh 1997; Dunowska et al. 2012). All arteriviruses share similar morphological and structural properties and replication and assembly strategies (Snijder et al. 2013). The EAV genome is approximately 12.7 kb in length and contains at least 10 known open reading frames (ORFs) (Balasuriya et al. 2013; Snijder et al. 2013). The 50-end is occupied by ORFs 1a and 1b, which encode two replicase polyproteins (pp1a and pp1ab). These two replicase polyproteins are further processed into at least 13 nonstructural proteins (nsp1-12, including nsp7 a/b). The remaining eight ORFs (2a, 2b, 3, 4, 5a, 5b, 6 and 7) are located at the 30-end of the genome and encode for the structural proteins of the virus (E, GP2, GP3, GP4, ORF5a protein, GP5, M, and N, respectively). The major envelope proteins (M and GP5) form a disulfide-linked heterodimer, while the minor envelope glycoproteins (GP2, GP3 and GP4) form a heterotrimer in the viral envelope (Balasuriya


et al. 2013; Snijder et al. 2013). The


unglycosylated E and ORF5a proteins are minor components of the viral particle. The reader is encouraged to refer to recent review articles by Balasuriya et al. (2013) and Snijder et al. (2013) for more details on molecular properties of the virus.


Epidemiology and transmission


As evidenced from serological surveys, EAV has a worldwide distribution primarily in domestic equine populations in North and South America, Europe, Australia, Africa, and various countries in Asia (Timoney and McCollum 1993). Other countries, such as Iceland, Japan, and New Zealand, are free of the disease (McFadden et al. 2013). Following the first recognition of EVA in 1953, outbreaks of the disease have also been reported from multiple countries including Switzerland, Austria, Poland, Italy, the UK, Ireland, Spain, the Netherlands, Canada, the United States, and Argentina (Burki 1970; McCollum and Bryans 1973; Gerber et al. 1978a; McCollum and Swerczek 1978; Timoney 1984; Golnik et al. 1986; Clayton 1987; Collins et al. 1987; Klavano 1987; Autorino et al. 1992; Cancellotti and Renzi 1992; Nowotny 1992; Camm and Thursby-Pelham 1993; Dwyer et al. 1993; Higgins 1993a,b; Timoney and McCollum 1993; van Gorkom et al. 1994;


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