Persistent infection and protection against Senecavirus A in pigs previously infected with a homologous and a heterologous isolate

Authors: PREIS, GUILHERME - University Of Minnesota; Buckley, Alexandra; WIESE, WENDY - University Of Minnesota; VANNUCCI, FABIO - University Of Minnesota

Submitted to: American Association of Swine Veterinarians Annual Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 9/4/2020
Publication Date: 2/18/2021
Citation: Preis, G., Devries, A.C., Wiese, W., Vannucci, F. 2021. Persistent infection and protection against Senecavirus A in pigs previously infected with a homologous and a heterologous isolate. American Association of Swine Veterinarians Annual Meeting. Poster No. 54.

Interpretive Summary:

Technical Abstract: The emergence of a vesicular disease in pigs in 2014/2015, caused by Senecavirus A (SVA), has been responsible for great concern due to its high similarity with reportable diseases such as foot-and-mouth disease. Despite the recent onset of SVA outbreaks in pig farms from different countries, the virus has been shown to be silently circulating in US herds since at least 1988. Preliminary data demonstrated the presence of virus in the tonsils of naturally infected pigs approximately 90 days after showing clinical disease, which suggests a potential for establishing persistent infections and an asymptomatic carrier state. In addition, there was no evidence whether animals previously exposed to a SVA strain are protected against homologous and heterologous isolates. Twenty-eight three weeks old crossbred gilts were allocated in three groups: group HC, inoculated with a historical followed by a contemporary isolate (n = 12); group CC, inoculated with a contemporary isolate in the two different time-points (n = 12); and group N, inoculated with RPMI medium (n = 4). Historical and contemporary isolates were obtained in 1999 and 2017 respectively. One animal from group CC died from an SVA-unrelated cause and was necropsied at 39 days post first inoculation (dpi). Two pigs from group N, three from group CC and four from HC were euthanized and necropsied at 49 dpi. The remaining pigs from groups HC and CC were re-challenged 50 days after the first inoculation. Oral swabs, fecal swabs and sera were collected for RT-qPCR, and sera was also submitted to indirect immunofluorescence (IFA) and serum neutralization (SN) assays. Shedding was determined when either oral or fecal swabs were positive by RT-qPCR. The time-points for collections were 1, 3, 7, 10, 14, 21, 28, 35, 42, 48, 52, 55, 57, 64 and 71 dpi. At day 71, the remaining pigs from all groups were necropsied. Tonsils of the soft palate, sub-mandibular and retropharyngeal lymph nodes from all pigs were submitted for RT-qPCR. Animals from groups HC and CC were shedding at day 3 dpi. Shedding started decreasing at days 10 and 14 dpi, with the last detections on days 28 and 35 dpi, for groups HC and CC, respectively. PCR positive serum was detected 3 dpi in both infected groups (12/12 HC and 11/12 CC) and persists until days 28 for group HC and 21 for group CC. Serological IgG response was first detected at 14 and 10 dpi in HC and CC groups, respectively. Two days after the second inoculation, 3/8 oral and 8/8 fecal swabs from both groups were positive by PCR, but there were no positive swabs in the following time-points. Viremia was observed in one pig from each of the HC and CC groups at 7 and 5 days after re-challenging, respectively. All pigs from groups HC and CC had at least one of the three collected tissues positive by RT-qPCR after necropsy, suggesting potential persistent infection, which should be further evaluated. Viral shedding after the first inoculation persisted up to 28 and 35 days in HC and CC groups, respectively, while viremia was consistently detected for 28 days from HC and 21 days from CC group. However, SVA was only detected two days after the second inoculation (52 dpi), with fewer animals being RT-qPCR positive in oral swabs than in fecal swabs. Since the animals were recently re-challenged, the higher positivity rate in fecal swabs may be due to detection of the inoculum. SN assays in serum collected be-fore the re-challenge demonstrated a higher average titer for the homologous strain used in each group. Additionally, a higher SN titer was seen in both groups when testing against both isolates in serum collected after re-challenge, suggesting a booster effect. These findings suggest that both groups re-challenged with homologous and heterologous strains showed protective immunity, characterized by limited viremia and shedding and increasing SN titers after re-