Experimental Seneca Valley virus infection in sows and their offspring

Authors: KIM, HANJUN - Iowa State University; Buckley, Alexandra; GUO, BAOQING - Iowa State University; KULSHRESHTHA, VIKAS - Regeneron Pharmaceuticals, Inc; VAN GEELEN, ALBERT - Animal And Plant Health Inspection Service (APHIS); MONTIEL, NESTOR - Animal And Plant Health Inspection Service (APHIS); Lager, Kelly; YOON, KYOUNG-JIN - Iowa State University

Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/17/2023
Publication Date: 12/20/2023
Citation: Kim, H., Devries, A.C., Guo, B., Kulshreshtha, V., Van Geelen, A., Montiel, N., Lager, K.M., Yoon, K. 2023. Experimental Seneca Valley virus infection in sows and their offspring. Veterinary Microbiology. https://doi.org/10.1016/j.vetmic.2023.109958.
DOI: https://doi.org/10.1016/j.vetmic.2023.109958

Interpretive Summary: Seneca Valley virus (SVV), also known as Senecavirus A, had been sporadically found in swine samples dating back to the late 1980s; however, in 2015 there was a sharp increase in detection related to cases of vesicular disease in swine. Vesicles are blister-like lesions that can progress to erosions typically found on the feet and snouts. In addition, on sow farms experiencing outbreaks of SVV and vesicular disease there were also reports of increased neonatal mortality. Clinical signs observed in piglets included lethargy, diarrhea, neurologic signs, and failure to thrive. Samples collected from clinical piglets have tested positive for SVV and negative for many other common pathogens responsible for disease in neonates. Scientists have been able to experimentally reproduce vesicular lesions in swine challenged in a research setting; however, there are no reports of scientists being able to reproduce clinical disease in neonates challenged with SVV. In order to gain a better understanding of the pathogenesis of SVV in sows and neonates, five sows were inoculated in late gestation and five sows and their piglets were inoculated shortly after farrowing. There was evidence of in utero infection in litters of two of the sows that were challenged in late gestation. In addition, two litters replicated virus after exposure to shedding from their respective sows after birth. None of the piglets that were directly challenged with the sows after farrowing demonstrated any significant clinical signs or mortality, though all had evidence of viral replication. In this study, we were unable to experimentally reproduce the clinical signs and mortality reported in neonates in the field during SVV outbreaks on sow farms. It is possible that another co-factor must be present for clinical disease to manifest such as additional pathogens or environmental stressors not present in a clean experimental setting. This study has provided a valuable information about the pathogenesis of SVV in sows and transmission of SVV from sows and their offspring that could be used to help shape SVV control measures in the swine industry.

Technical Abstract: There have been reports of increased neonatal mortality on swine breeding farms experiencing swine idiopathic vesicular disease (SIVD) outbreaks, which can be accompanied by lethargy, diarrhea, and neurologic signs in neonates. Seneca Valley Virus (SVV), or Senecavirus A, has been detected in clinical samples taken from pigs with SIVD. Experimental SVV inoculation has caused vesicular disease in pigs, particularly during the stages from weaning to finishing. However, it remains crucial to investigate whether SVV directly contributes to the increase in neonatal mortality rates. The following study was conducted to chronicle the pathogenesis of SVV infection in sows and their offspring. Ten sows were intranasally inoculated with 4.75×107 plaque-forming units of the virus per sow either late in gestation (n=5) or within fourteen days of farrowing (n=5). Each sow replicated SVV following intranasal inoculation, but only one out of ten sows developed a vesicular lesion on the snout. Evidence of transplacental infection was observed in two litters, and an additional two litters became infected following parturition out of five litters from sows inoculated in late gestation. No clinical signs were observed in the infected neonates. Likewise, no clinical signs were observed in the other five litters inoculated after farrowing, although each piglet did replicate the challenge virus. In this study, experimental challenge of SVV did not result in neonatal mortality in contrast to observations in the field; however, it has shed light on pathogenesis of the virus, transmission of SVV between sows and their offspring, and host immune response that can help shape control measures in the field.