Abstract

In this study, we analyzed PRRS virus (PRRSv) specific lymphocyte function in piglets vaccinated with Ingelvac PRRSFLEX EU® at two and three weeks of age in the presence of homologous maternal immunity. Complete analysis of maternal immunity to PRRSv was evaluated postpartum, as well as passive transfer of antibodies and T cells to the piglet through colostrum intake and before and after challenge with a heterologous PRRSv at ten weeks of age. Maternal-derived antibodies were detected in piglets but declined quickly after weaning. However, vaccinated animals restored PRRSv-specific antibody levels by anamnestic response to vaccination. Cell analysis in colostrum and milk revealed presence of PRRSv-specific immune cells at suckling with higher concentrations found in colostrum than in milk. In addition, colostrum and milk contained PRRSv-specific IgA and IgG that may contribute to protection of newborn piglets. Despite the presence of PRRSv-specific Peripheral Blood Mononuclear cells (PBMCs) in colostrum and milk, no PRRSv-specific cells could be detected from blood of the piglets at one or two weeks of life. Nevertheless, cellular immunity was detectable in pre-challenged piglets up to 7 weeks after vaccination while the non-vaccinated control group showed no interferon (IFN) γ response to PRRSv stimulation. After challenge, all piglets developed a PRRSv-specific IFNγ-response, which was more robust at significantly higher levels in vaccinated animals compared to the primary response to PRRSv in non-vaccinated animals. Cytokine analysis in the lung lumen showed a reduction of pro-inflammatory responses to PRRSv challenge in vaccinated animals, especially reduced interferon (IFN) α levels. In conclusion, vaccination of maternally positive piglets at 2 and 3 weeks of age with Ingelvac PRRSFLEX EU induced a humoral and cellular immune response to PRRSv and provided protection against virulent, heterologous PRRSv challenge.

Highlights

  • The porcine reproductive and respiratory syndrome (PRRS) is caused by an enveloped RNA virus affecting pigs worldwide and leading to great economic losses in the swine industry [1]

  • These results suggest that vaccination at 2 or 3 weeks of life was conducted in the full presence of PRRS viruses (PRRSv)-specific maternally derived antibodies (MDA)

  • In contrast to the non-vaccinated control group both vaccinated groups showed a constant level of anti-PRRSv antibodies in their blood indicating that acquired humoral immunity through vaccination with Ingelvac PRRSFLEX EU filled the gap of consistently declining maternal antibody levels

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Summary

Introduction

The porcine reproductive and respiratory syndrome (PRRS) is caused by an enveloped RNA virus affecting pigs worldwide and leading to great economic losses in the swine industry [1]. Infections can occur in pigs of all ages, provoking respiratory syndromes, cyanosis of extremities as well as reproductive failure in sows [2]. Similarities exist between and within the PRRSv-1 strains, there is enough diversity that vaccines may not induce sufficient cross-protection against heterologous strains [7]. Vaccination with a modified life virus (MLV) against PRRSv has been demonstrated as an effective tool to control clinical signs related to infection [9, 10], while killed virus (KV) vaccines, when used for priming, could not induce an effective protection against the clinical outcome of disease [11]

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