Pathogenesis of Pseudorabies Virus in Mouse Placenta Insights into Maternal Infant Transmission Mechanisms

Pseudorabies virus infection poses a significant threat to reproductive success in pregnant animals, often resulting in miscarriage and stillbirth. To elucidate the mechanisms underlying PRV vertical transmission, we established a PRV infection model in pregnant mice. PRV was detected in the placental trophoblast layer, indicating trans placental transmission via maternal circulation. Mechanistically, PRV disrupts tight junctions within the placental barrier, facilitating viral entry into fetal tissues.Infection also reduces maternal progesterone levels and impairs placental vascular development, thereby compromising maternal fetal exchange. Histological and molecular analyses revealed increased apoptosis, inflammatory cytokine expression, and oxidative stress in placental tissues. Transcriptomic profiling demonstrated the activation of pathways related to inflammation, oxidative stress, and apoptosis, as well as the enrichment of pathways involved in hormone synthesis, angiogenesis, and trophoblast development. Several key regulators of trophoblast proliferation and differentiation were significantly downregulated.These findings reveal that PRV compromises placental integrity and function through multiple pathogenic pathways, providing mechanistic insights into its vertical transmission and associated pregnancy failure.