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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Virus and Prion Research » Research » Publications at this Location » Publication #326790

Title: Demonstration of Senecavirus A protective immunity in a pig model

Author
item BUCKLEY, ALEXANDRA - Oak Ridge Institute For Science And Education (ORISE)
item MONTIEL, NESTOR - Oak Ridge Institute For Science And Education (ORISE)
item KULSHRESHTHA, VIKAS - Oak Ridge Institute For Science And Education (ORISE)
item VAN GEELEN, ALBERT - Oak Ridge Institute For Science And Education (ORISE)
item GUO, BAOQING - Iowa State University
item HOANG, HAI - Iowa State University
item RADEMACHER, CHRISTOPHER - Iowa State University
item YOON, KYOUNG-JIN - Iowa State University
item Lager, Kelly

Submitted to: International Pig Veterinary Society (IPVS)
Publication Type: Abstract Only
Publication Acceptance Date: 3/1/2016
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Although idiopathic vesicular disease (IVD) is rarely diagnosed in US swine, in 2015 there were over 100 cases identified throughout the country. Frequently, Senecavirus A (SVA) has been associated with IVD and is presumed to be the etiologic agent. In recent studies we have shown SVA to induce a vesicular disease in nursery and finishing age pigs. This paper describes initial efforts demonstrating SVA protective immunity. Two litters of pigs (n=10, n=6) were used at 1 and 7 days-of-age, respectively (time = D0). On D0, one-half of each litter was weaned into a separate room (Group A). Each remaining half (Group B) was kept with their dam until D14, and each pig and both sows received an intranasal inoculation of the 15-41901SD SVA isolate (5x107 pfu/pig). Serum and swabs samples were collected from Group B pigs at D4, 10 and 20. On D45, all piglets in both groups received an intranasal inoculation of the same viral stock at the same dose. Clinical observations, serum and swab samples were collected at D45, 47, 49, 52, and 54 at which time all pigs were euthanized. Sows were euthanized on D14. All serum and swab samples were tested for SVA by PCR. In Group B pigs on D4 SVA was detected in 8/8, 7/8, and 8/8 serum, fecal and oral swab samples, respectively. On D10, SVA was detected in 3/8, 6/8, and 8/8 serum, fecal and oral swab samples, respectively. No SVA was detected in any sample on D20. No cutaneous lesions were observed in Group B. In sows, a PCR positive serum and fecal swab were detected in one sow on D10, all other samples from either sow (D4, D10, D14) were negative. On D8 a sow developed a vesicle on her snout, no other cutaneous lesions were observed in either sow. Following challenge at D45, all Group A pigs were PCR positive in one or more samples on each day. All Group A pigs developed one or more cutaneous lesions located on coronary band, interdigital space, or tongue by D54. SVA was detected in vesicular lesions. In contrast, none of the pigs in Group B were PCR positive, nor developed any cutaneous lesions following second SVA challenge. Prior SVA infection of neonatal pigs induced a homologous protective immunity when tested 45 days later demonstrating young pigs can be used as a model to study the SVA immune response.