نبذة مختصرة : Competing Interests: Declarations. Ethics approval and consent to participate: All animal work was approved by the University of Saskatchewan’s Animal Research Ethics Board (Protocol # 20160023). Animals were purchased from a commercial company for this study. Consent for publication: Not applicable. Competing interests: Dr. Joan Lunney, an author on this manuscript, is a member of the editorial board for the BMC Genomics journal.
Background: Porcine reproductive and respiratory syndrome virus (PRRSV) can be transmitted across the maternal-fetal-interface from an infected gilt to her fetuses. Although fetal infection status and disease outcomes vary, the mechanisms are not completely understood. The objective was to assess targeted placental structural and transporter-related gene expression patterns. At day 85 of gestation pregnant pigs were challenged with PRRSV, and at 12 days post maternal infection sows and fetuses were sacrificed, and the placental tissue was collected. Grouping of fetuses was by preservation status and PRRS viral load (VL): control (CTRL, n = 14), viable and low VL fetus (VIA_LVF, n = 15), viable and high VL fetus (VIA_HVF, n = 21), meconium mild and low VL fetus (MECm_LVF, n = 14), meconium mild and high VL fetus (MECm_HVF, n = 14), and meconium severe and high VL fetus (MECs_HVF, n = 13). NanoString was used to evaluate the expression of 86 genes: actin cytoskeleton signaling, arachidonic acid pathway, integrin signaling, intercellular junctions, transporters, and VEGF signaling. Statistical analyses were performed using Limma with P ≤ 0.05 considered significant.
Results: We identified 1, 7, 0, 29, and 39 differentially expressed genes in VIA_LVF, VIA_HVF, MECm_LVF, MECm_HVF, and MECs_HVF, respectively, contrasted to CTRL. Placental transporter genes were significantly impacted (i.e., downregulation of SLC1A3, SLC1A5, SLC2A1, SLC2A3, SLC2A5, SLC2A10, SLC2A12, SLC7A4, SLC16A5, SLC16A10, and SLC27A6; and upregulation of SLC2A2, SLC16A3, and SLC27A4), compared to CTRL. Actin cytoskeleton signaling (ARHGEF6 and ARHGEF7), arachidonic acid (PTGES3 and PTGIS), integrin signaling (FN1 and ITGB6), intercellular junctions (CDH3 and CDH11), and VEGF signaling (MAPK3 and HPSE) gene groupings were significantly impacted, compared to CTRL.
Conclusion: Data reported here indicate that fetal PRRSV infection levels rather than fetal demise is necessary for transcriptional dysregulation of the fetal placenta, with a tendency towards more downregulation in the target gene sets among susceptible fetuses. These results generally support that in susceptible fetuses there is altered solute transportation, placental structural integrity, and reduced angiogenesis. The data described here is associated with fetal PRRS resistance/resilience and susceptibility.
(© 2025. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)
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