Identification of linear B cell epitopes on VP1 and VP2 proteins of Senecavirus A (SVA) using monoclonal antibodies.

Senecavirus A (SVA), previously called Seneca Valley virus, belongs to the family Picornaviridae, species Senecavirus A, in the Senecavirus genus, and can cause vesicular lesions in sows and acute death in piglets. In this study, recombinant VP1 and VP2 proteins were expressed in prokaryotic expression system and used to generate eight monoclonal antibodies (mAbs) against VP1 or VP2 protein. And all of the mAbs reacted specifically with SVA virus by both Western blot and indirect immunofluorescence assay (IFA). The resurts showed that all of the epitopes aganist these mAbs were B cell linear epitopes. To map the epitopes, both Western blot and indirect enzyme-linked immunosorbant assay (indirect ELISA) were performed. The epitope 21GELAAP26 recognized by mAb 1G9, was likely to be a significant B cell epitope due to the high antigenic index and the fully exposure on the surface of the VP1. Other mAbs were recognized by VP2 protein. MAbs 1E7 and 8E8 recognized the same epitope at 12DRVITQT18, 1A5 recognized the epitope at 71WTKAVK76, 1G2 recognized the epitope at 98GGAFTA103, 9D2 and 6B11 recognized the same epitope at 150KSLQELN156, and 7E4 recognized the epitope at 248YKEGAT253. Alignment of amino acids revealed that four epitopes were completely conserved among all SVA strains, including 21GELAAP26, 71WTKAVK76, 98GGAFTA103, and 248YKEGAT253. Interestingly, there were some amino acid mutations in 12DRVITQT18 and 150KSLQELN156, but no significant difference was detected on the reaction intensity between epitopes and the corresponding mAbs. This is the first report about the SVA epitopes, which will benefit to the study of viral pathogenic mechanism, vaccine design, as well as the establishment of detection methods.

Pathogenesis of a senecavirus a isolate from swine in shandong Province, China.

Senecavirus A (SVA), previously called Seneca Valley virus, can cause vesicular lesions in sows and a sharp decline in neonatal piglet production. In this study, a SVA strain was isolated from a pig herd in Shandong Province in China and identified as SVV-CH-SD. The full genome was 7286 nucleotides (nt) in length and contained a single open reading frame (ORF) of 6546 nt, encoding a 2182 amino acid (aa). A phylogenetic analysis showed that the isolate shares highest sequence homology (98.52 %) with SVA strain USA-GBI26-2015. A genetic comparison of virulent and weakly virulent SVA strains showed that some amino acid residues may be associated with virulence. Animal challenge experiments showed that 90-100-day-old pigs inoculated with SVV-CH-SD intraorally and intranasally, intranasally, or intramuscularly developed low fever, blisters, and lameness. They had similar levels of neutralizing antibodies against SVA and viral loads in the serum and organs at 28 days post-CHallenge. However, 30-35- and 55-65-day-old pigs challenged with SVV-CH-SD showed no clinical signs, although anti-SVA neutralizing antibodies were detected. Our findings provide useful data for studying the pathogenesis and transmission of SVA in pigs.