Abstract
The porcine reproductive and respiratory syndrome (PRRS) is a devastating viral disease affecting swine production, health and welfare throughout the world. A synergistic action of the innate and the adaptive immune system of the host is essential for mounting a durable protective immunity through vaccination. Therefore, the current study aimed to investigate the transcriptome profiles of peripheral blood mononuclear cells (PBMCs) to characterize the innate and the adaptive immune response to PRRS Virus (PRRSV) vaccination in Pietrain pigs. The Affymetrix gene chip porcine gene 1.0 ST array was used for the transcriptome profiling of PBMCs collected at immediately before (D0), at one (D1) and 28 days (D28) post PRRSV vaccination with three biological replications. With FDR <0.05 and log2 fold change ±1.5 as cutoff criteria, 295 and 115 transcripts were found to be differentially expressed in PBMCs during the stage of innate and adaptive response, respectively. The microarray expression results were technically validated by qRT-PCR. The gene ontology terms such as viral life cycle, regulation of lymphocyte activation, cytokine activity and inflammatory response were enriched during the innate immunity; cytolysis, T cell mediated cytotoxicity, immunoglobulin production were enriched during adaptive immunity to PRRSV vaccination. Significant enrichment of cytokine-cytokine receptor interaction, signaling by interleukins, signaling by the B cell receptor (BCR), viral mRNA translation, IFN-gamma pathway and AP-1 transcription factor network pathways were indicating the involvement of altered genes in the antiviral defense. Network analysis revealed that four network modules were functionally involved with the transcriptional network of innate immunity, and five modules were linked to adaptive immunity in PBMCs. The innate immune transcriptional network was found to be regulated by LCK, STAT3, ATP5B, UBB and RSP17. While TGFß1, IL7R, RAD21, SP1 and GZMB are likely to be predictive for the adaptive immune transcriptional response to PRRSV vaccine in PBMCs. Results of the current immunogenomics study advances our understanding of PRRS in term of host-vaccine interaction, and thereby contribute to design a rationale for disease control strategy.
Highlights
Porcine reproductive and respiratory syndrome virus (PRRSV) is the causative agent of an economically important swine disease, which is clinically characterized by reproductive failure in pregnant sows and respiratory disorder in young pigs [1]
This study support a model in which peripheral blood mononuclear cells (PBMCs) transcriptome alterations are involved in upregulation of CD28 dependent VAV1 pathway, signaling by interleukins and ubiquitination pathway at the initial 24 hours after vaccination; and upregulation of IL12-mediated signaling events, AP-1 transcription factor network and TGF-beta receptor signaling pathways at 28 days after PRRSV vaccination in pigs
Among the vaccine induced genes, lymphocyte-specific protein tyrosine kinase (LCK), STAT3, ATP5B, UBB and RSP17 were found to be the potential candidates for innate immune responses to PRRSV vaccine in the peripheral blood
Summary
Porcine reproductive and respiratory syndrome virus (PRRSV) is the causative agent of an economically important swine disease, which is clinically characterized by reproductive failure in pregnant sows and respiratory disorder in young pigs [1]. The common symptoms to PRRSV infection has been characterized by prolonged viremia, a deficient induction of innate immunity along with weak and delayed development of neutralizing antibodies [2, 3] which are the major hurdle for control of porcine reproductive and respiratory syndrome (PRRS). Elucidating the main genomic factors involved in developing protective immune response to PRRSV vaccination is of utmost importance. The virulent PRRSV infection causes depletion of immune cells through cytophathic replication preferably within the alveolar macrophage. The quality of immunity derived from natural PRRSV infection seemed not ideal for the implementation in the vaccine development programs [9] that provoked the molecular characterization of host-vaccine interaction
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