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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #360225

Research Project: Intervention Strategies to Control Endemic and New and Emerging Viral Diseases of Swine

Location: Virus and Prion Research

Title: Efficacy of an inactivated Seneca Valley virus vaccine in nursery-aged pigs

item BUCKLEY, ALEXANDRA - Oak Ridge Institute For Science And Education (ORISE)
item PATTERSON, ABBY - Boehringer Ingelheim
item VAN GEELEN, ALBERT - Orise Fellow
item Lager, Kelly

Submitted to: Vaccine
Publication Type: Abstract Only
Publication Acceptance Date: 11/15/2018
Publication Date: 2/1/2018
Citation: Buckley, A., Patterson, A., Van Geelen, A., Lager, K.M. 2018. Efficacy of an inactivated Seneca Valley virus vaccine in nursery-aged pigs. Vaccine. 36(6):841-846.

Interpretive Summary:

Technical Abstract: Introduction Senecavirus A, commonly known as Seneca Valley virus (SVV), causes vesicular disease in swine that is clinically indistinguishable from foot-and-mouth disease (FMD). Therefore, when a vesicle is observed, a foreign animal disease investigation must be performed by trained personnel. These investigations have economic ramifications for federal and state governments investigating the case as well as for producers and packers who cannot move animals with active lesions. A vaccine that provides clinical protection from SVV infection could be a valuable tool for the swine industry to improve swine health and reduce disruptions related to foreign animal disease investigations. Materials and Methods Weaned pigs were split into 4 groups: Group 1 (no vax + sham, n=8), Group 2 (no vax + challenge, n=15), Group 3 (vax + sham, n=8) and Group 4 (vax + challenge, n=15). At 4 and 7 weeks-of-age Groups 3 and 4 were vaccinated intramuscularly (IM) with 2 mL of whole-virus inactivated SVV with an oil-in-water emulsion adjuvant. Pigs were intranasally challenged at 9 weeks-of-age (0 dpc) with 5 mL of SVV (10*6 TCID50/mL, challenge) or Minimum Essential Medium (sham). All pigs were rectal swabbed daily for the first 10 dpc and checked for vesicular lesions. Pigs were bled at -42, -21, 0, 3, 5, 7, 14, and 21 dpc. Rectal swabs and serum were tested for SVV RNA by PCR and the antibody response was determined by virus neutralization (VN) assay. Results In Group 1 (no vax + sham), there were no clinical signs, SVV RNA was not detected in serum or feces by PCR, and none of the pigs developed a neutralizing antibody response. In Group 2 (no vax + challenge), 80% had vesicular lesions, SVV RNA was detected in serum in most animals (from 1-7 dpc), and 80% of pigs had detectable SVV RNA in rectal swabs by 1 dpc with shedding detected until 21 dpc in 60% of pigs. No animals had a VN titer greater than 1:16 prior to challenge (0 dpc) and after challenge titers ranged from 1:16 to 1:256. In Group 3 (vax + sham), all animals developed a VN titer of 1:256 following two doses of vaccine (21 dpc). Following sham challenge, no animals had vesicular lesions and SVV RNA was never detected in serum or fecal samples. In Group 4 (vax + challenge), all animals had VN titers between 1:64 and 1:1024 following two doses of vaccine (21 dpc). Following virulent challenge, no animals had vesicular lesions and SVV RNA was never detected in serum. However, SVV RNA was detected in fecal samples in 13/15 pigs on 1 dpc, but all were negative by 2 dpc. Conclusion Whole-virus inactivated SVV plus an oil-in-water emulsion adjuvant provided protection against clinical disease and prevented viremia. While viral nucleic acid was detected in rectal swabs from vaccinated animals on 1-2 dpc, it is not known if this material was passed through from the intranasal inoculation or reflective of active replication within the pig. Moreover, it is not known if this material was infectious. An effective vaccine could have a positive impact on welfare in the swine industry and reduce the economic burden of investigating vesicular disease.