Abstract
BackgroundPorcine reproductive and respiratory syndrome (PRRS) is one of the most economically important viral diseases affecting swine industry worldwide. Despite routine farm vaccination, effective control strategies for PRRS remained elusive which underscores the need for in-depth studies to gain insight into the host immune response to vaccines. The current study aimed to investigate transcriptional responses to PRRS Virus (PRRSV) vaccine in the peripheral blood mononuclear cells (PBMCs) within 3 days following vaccination in German Landrace pigs.ResultsTranscriptome profiling of PBMCs from PRRSV vaccinated and age-matched unvaccinated pigs at right before (0 h), and at 6, 24 and 72 h after PRRSV vaccination was performed using the Affymetrix gene chip porcine gene 1.0 st array. Comparison of PBMCs transcriptome profiles between vaccinated and unvaccinated pigs revealed a distinct host innate immune transcriptional response to PRRSV vaccine. There was a significant temporal variation in transcriptional responses of PRRSV vaccine in PBMCs accounting 542, 2,263 and 357 differentially expressed genes (DEGs) at 6, 24 and 72 h post vaccination, respectively compared to the time point before vaccination (controls). Gene ontology analysis revealed the involvement of these DEGs in various biological process including innate immune response, signal transduction, positive regulation of MAP kinase activity, TRIF-dependent toll-like receptor signaling pathway, T cell differentiation and apoptosis. Immune response specific pathways such as cytokine-cytokine receptor interaction, chemokine signaling pathway, signal transduction, JAK-STAT pathway and regulation, TRAF6 mediated induction of NF-kB and MAPK, the NLRP3 inflammasome, endocytosis and interferon signaling were under regulation during the early stage of PRRSV vaccination. Network enrichment analysis revealed APP, TRAF6, PIN1, FOS, CTNNB1, TNFAIP3, TIP1, CDKN1, SIRT1, ESR1 and HDAC5 as the highly interconnected hubs of the functional network of PRRSV vaccine induced transcriptome changes in PBMCs.ConclusionsThis study showed that a massive gene expression change occurred in PBMCs following PRRSV vaccination in German Landrace pigs. Within first 3 days of vaccine exposure, the highest transcript abundance was observed at 24 h after vaccination compared to that of control. Results of this study suggest that APP, TRAF6, PIN1, FOS, CDKN1A and TNFAIP3 could be considered as potential candidate genes for PRRSV vaccine responsiveness.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2849-1) contains supplementary material, which is available to authorized users.
Highlights
Porcine reproductive and respiratory syndrome (PRRS) is one of the most economically important viral diseases affecting swine industry worldwide
PRRS Virus (PRRSV)-specific antibody responses In order to exclude the maternally derived antibody (MDA) response of PRRSV as well as to evaluate the vaccine induced antibody response, plasma samples from all pigs at day 7, 28, 42, 56 and 70 of age were screened by ELISA
The plasma antibody level confirmed that experimental pigs were negative for MDA of PRRSV considering the sample to positive (s/p) ratio of 0.4 (40 %) as threshold (Fig. 1)
Summary
Porcine reproductive and respiratory syndrome (PRRS) is one of the most economically important viral diseases affecting swine industry worldwide. The current study aimed to investigate transcriptional responses to PRRS Virus (PRRSV) vaccine in the peripheral blood mononuclear cells (PBMCs) within 3 days following vaccination in German Landrace pigs. The disease is caused by an enveloped, positive-sense, singlestranded RNA virus called porcine reproductive and respiratory syndrome virus (PRRSV). Some of the non-structural proteins (Nsp, Nsp, Nsp11) and a structural protein (N protein) of PRRSV are known to be associated with IFN suppression in the infected cells [4]. The RIG-I/MDA5 and JAK-STAT pathways are two major signaling pathways for IFN production which are found to be impaired by PRRSV during acute infection [4]. The timing and the potency of the host cellular and immunological events that occur following infection are likely potential determinants governing the pathogenesis [9]
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