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Monreal et al. 1995; Wood et al. 1995; Balasuriya et al. 1998; McCollum et al. 1998; Echeverria et al. 2003; Olguin Perglione et al. 2010). However, EAV seroprevalence varies between countries and between horses of different breeds and ages within the same country. In the USA, a very high percentage of adult Standardbred and Saddlebred horses are seropositive for EAV (70–90% and 8–25%, respectively), whereas the seroprevalence in the Thoroughbred population is very low (<5.4%) (McCollum and Bryans 1973; Timoney and McCollum 1988, 1993; McCue et al. 1991; McKenzie 1996). The 1998 National Animal Health Monitoring System (NAHMS) equine survey showed that only 0.6% of the US American Quarter Horse population was seropositive to EAV (NAHMS 2000), but the extensive multistate EVA occurrence in the USA during 2006–2007 has probably increased the seroprevalence within this breed (Zhang et al. 2010b). The seroprevalence in Warmblood stallions is also very high in several European countries, with some 55–93% of Austrian Warmblood stallions being seropositive for EAV (Moraillon and Moraillon 1978; Burki et al. 1992). Similarly, there is a high seroprevalence among mares and stallions of Hucul horses in Poland (53.2 and 68.2%, respectively) (Rola et al. 2011), and a recent study performed in a population of Spanish purebred horses demonstrated a seroprevalence of 17.3% (Cruz et al. 2015). Seroprevalence of EAV increases with age, indicating that horses may be repeatedly exposed to the virus during their lifespan. In addition, several studies have identified a correlation between the number of breeding mares and EAV seropositivity (Timoney and McCollum 1993; Cruz et al. 2015). Differences in the breed-specific seroprevalence of EAV
infection may reflect genetic differences that confer resistance to infection. Recent studies have suggested that there is a genetic difference between stallions that become long-term carriers and those that clear the virus from the reproductive tract shortly after infection (Go et al. 2012a). This trait was linked to the susceptibility of CD3+ T lymphocytes to in vitro EAV infection and a common dominant haplotype located in equine chromosome 11 (ECA11; position 49572804–49643932) (Go et al. 2010, 2011a, 2012a). Thus, these studies suggest that those stallions with an in vitro CD3+ T lymphocyte susceptible phenotype are at a higher risk of becoming long-term carriers after EAV infection than those that have a resistant one (Go et al. 2012a).
Transmission of EAV between horses occurs through either
respiratory or venereal routes (Doll et al. 1957b; McCollum et al. 1971; Cole et al. 1986; Timoney et al. 1986, 1987a; Timoney and McCollum 1993). Horizontal transmission occurs through the respiratory route after aerosolisation of viral particles in respiratory secretions originating from acutely infected horses and is facilitated by direct and/or close contact between an infected and a na€ıve horse (Fig 1). Nasal shedding of EAV frequently lasts 7–14 days during the acute phase of the infection, with viral titres ranging from 10 to >2 9 103 plaque-forming units per mL (PFU/mL) (McCollum et al. 1971, 1988; Balasuriya et al. 1999b). EAV can also be spread by aerosolised urine and other body secretions and excretions of acutely infected horses, aborted fetuses, and fetal membranes (McCollum et al. 1971, 1995; McCollum 1981; Burki et al. 1992; Glaser et al. 1996, 1997; Guthrie et al. 2003). It has been demonstrated that EAV is shed in faeces of experimentally infected stallions up to 8 days post-infection (Neu et al. 1988), and the virus is also present in the female
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reproductive tract for a brief period after infection (McCollum et al. 1988). Furthermore, EAV may be transmitted indirectly by carrier stallions to seronegative, susceptible stallions by masturbation (Guthrie et al. 2003). The venereal mode of transmission occurs exclusively via
semen from acutely or chronically infected stallions (carrier stallions) during natural or artificial breeding (Timoney et al. 1987a). Following infection, 10–70% of EAV infected stallions become persistently infected and continuously shed virus in their semen for a variable and frequently extended period of time, ranging from several weeks to years post-infection or even life-long, despite the presence of high levels of neutralising antibodies in serum (Timoney et al. 1986, 1987a; Timoney and McCollum 1993) (Fig 1). Currently, there are no means of estimating when the EAV carrier state is likely to be eliminated by a carrier stallion. Carrier stallions play a major epidemiological role since they constitute the natural reservoir for EAV and, thus, are responsible for the maintenance, perpetuation, and evolution of EAV in equine populations between breeding seasons (Timoney and McCollum 1988, 1993; Balasuriya et al. 1999a, 2001, 2004a; Hedges et al. 1999; Zhang et al. 2010a; Miszczak et al. 2012). Several studies have shown that EAV carrier stallions are a source of genetic and phenotypic divergence for the virus, i.e. EAV evolves in the reproductive tract of carrier stallions resulting in the emergence of novel viral variants with neutralisation phenotypes that allow immune escape and which can lead to outbreaks of EVA (Balasuriya et al. 1999a, 2001, 2004a; Hedges et al. 1999). Most of the seronegative mares naturally or artificially
bred to carrier stallions become infected and seroconvert within 28 days (Timoney et al. 1987b; McCollum et al. 1988; Balasuriya et al. 1998). Infected mares may develop clinical signs of EVA; irrespective of clinical status, acutely infected mares can readily transmit the virus by the respiratory route to susceptible cohorts in close proximity and can rapidly initiate an EVA outbreak (Fig 1). It has been demonstrated that EAV can be transmitted from donor mares inseminated with EAV- infective semen to na€ıve recipient mares via embryo transfer (Broaddus et al. 2011a). Furthermore, congenital infection of foals following transplacental transmission of the virus in mares infected in late gestation can occur, and congenitally infected foals develop a rapidly progressive, fulminating interstitial pneumonia and fibrinonecrotic enteritis (Golnik et al. 1981; Carman et al. 1988; Vaala et al. 1992; Wilkins et al. 1995; Del Piero et al. 1997). Lateral transmission of EAV can also occur through contaminated fomites (e.g. personnel, clothing, vehicles and equipment such as artificial vaginas and phantoms) (Timoney and McCollum 1988, 1993; Guthrie et al. 2003). Equine arteritis virus is highly heat labile and its half-life
80°C) for more than 6 decades without any significant loss of virus infectivity (U.B.R. Balasuriya and P.J. Timoney, unpublished data). The virus can also remain viable in tissue
progressively decreases with increasing temperature. The virus is readily inactivated by lipid solvents (such as ether and chloroform) and by common disinfectants and detergents. EAV remains infectious for 75 days at 4°C, for 2–3 days at 37°C, and 20–30 min at 56°C (de Vries 1994). EAV-infected tissue samples, tissue culture fluid, semen samples and embryos can be stored frozen (70°Cto
samples stored at 20°C for more than 5 years (McCollum et al. 1961).
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