Evaluation of Senecavirus A transmission in laboratory and wild type mice strains under experimental conditions

摘要

Senecavirus A (SVA) is a non-enveloped, single-stranded RNA virus of the genus Senecavirus in the family Picornaviridae.1 The virus possesses four structural proteins (VP 1 -4) composing its icosahedral capsid, and seven non-structural proteins.2 Seneca Valley Virus (S W) was discovered as a contaminant in cultured cells in 2002 and demonstrated oncolytic properties. SVA has been documented retrospectively in serum from United States' swine back to 1988.3 SW was renamed SVA, and contemporary strainshave recendy been identified as the causative agent of outbreaks of porcine idiopathic vesicular disease (IVD) and epidemic transient neonatal losses (ETNL) in swine production systems. Increased incidence was observed in the United States beginning in 201^6 The disease has also been reported in Canada,7 Brazil,8 China,9 Colombia,10 and Thailand." Outbreaks of SVA IVD are characterized by abrupt onset of vesicles that progress to ulcerative dermatitis on the nostril and coronary bands in a high percentage of sows or finisher pigs. Animal present with transient fever, off feed, and most importandy lameness. However, SVA can be difficult to diagnose because both clinical signs and lesions are transient. Outbreaks in 2015 and 2016 showed recurrent seasonal patterns, with increased cases load in mid-summer tapering through the fall. Lesions associated with SVA are clinically indistinguishable from those observed in foot-and-mouth disease (FMD), vesicular stomatitis (VS), swine vesicular disease (S VD), and vesicular exanthema of swine (VES). Clinically unaffected animals at sites experiencing outbreaks showed S VA-specific antibody response, suggesting that the virus may circulating subclinically.