Abstract
Porcine epidemic diarrhea virus strains from the G1b cluster are considered less pathogenic compared to the G2b cluster. The aim of this study was to compare the ability of G1b-based live virus exposure against use of a commercial G2b–based inactivated vaccine to protect growing pigs against G2b challenge. Thirty-nine PEDV naïve pigs were randomly divided into five groups: EXP-IM-1b (intramuscular G1b exposure; G2b challenge), EXP-ORAL-1b (oral G1b exposure; G2b challenge), VAC-IM-2b (intramuscular commercial inactivated G2b vaccination; G2b challenge), POS-CONTROL (sham-vaccination; G2b challenge) and NEG-CONTROL (sham-vaccination; sham-challenge). Pigs were vaccinated/exposed at 3 weeks of age (day post-vaccination 0, dpv 0), VAC-IM-2b pigs were revaccinated at dpv 14, and the pigs were challenged at dpv 28. Among all groups, VAC-IM-2b pigs had significantly higher anti-PEDV IgG levels on dpv 21 and 28 while EXP-ORAL-1b pigs had significantly higher anti-PEDV IgA levels on dpv 14, 21, 28 and 35. EXP-ORAL-1b also had detectable IgA in feces. Intramuscular PEDV exposure did not result in a detectable antibody response in EXP-IM-1b pigs. The fecal PEDV RNA levels in VAC-IM-2b pigs were significantly lower 5–7 days after challenge compared to the POS-CONTROL group. Under the study conditions a commercial inactivated G2b-based vaccine protected pigs against G2b challenge, as evidenced by reduction of PEDV RNA in feces for 3–4 logs during peak shedding and a shorter viral shedding duration. The oral, but not the intramuscular, experimental G1b-based live virus exposure induced a high anti-PEDV IgA response prior to challenge, which apparently did not impact PEDV shedding compared to POS-CONTROL pigs.
Highlights
Clinical porcine epidemic diarrhea and its causative virus PEDV were discovered in European pigs in the 1970s [1, 2], spread to Asia during the 1980s and 1990s [3], and became endemic in pigs on both continents [2, 3]
G1a includes historic PEDV isolates such as CV777 and attenuated variants distributed in Europe and Asia, whilst G1b includes the so called S-INDEL strains which can be found in Europe, Asia and North America
At 3 weeks of age or dpv 0, EXP-IM-1b, EXP-ORAL-1b and VAC-IM-2b groups were vaccinated with different vaccines and routes as outlined in Table 1, whereas POS-CONTROL and NEG-CONTROL pigs were sham-vaccinated with saline
Summary
Clinical porcine epidemic diarrhea and its causative virus PEDV were discovered in European pigs in the 1970s [1, 2], spread to Asia during the 1980s and 1990s [3], and became endemic in pigs on both continents [2, 3]. 10 years ago PEDV re-emerged as an important enteric disease of suckling and growing pigs [4]. In 2013, PEDV was introduced for the first time to North America [5] causing major disease and mortality [6]. On the basis of Spike (S) gene sequences, PEDV isolates can be divided into G1a, G1b, G2a and G2b [7, 8]. G1a includes historic PEDV isolates such as CV777 and attenuated variants distributed in Europe and Asia, whilst G1b includes the so called S-INDEL strains which can be found in Europe, Asia and North America. G2a isolates are restricted to Asia whereas G2b isolates are present in Asia and the Ukraine [9], and since US introduction
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