Pathogenesis of pseudorabies virus in mouse placenta: insights into maternal-infant transmission mechanisms

Pseudorabies virus (PRV) infection poses a significant threat to reproductive success in pregnant pigs, often leading to abortion and stillbirth. Systematic studies on the vertical transmission mechanism of PRV through the placenta remain limited. To address this research gap, we developed a PRV infection model in pregnant mice. Immunohistochemical analysis detected strong PRV-positive signals in placental trophoblasts and fetal brains, with viral loads significantly higher than those in the maternal bloodstream. These results suggest that PRV can infect the placenta via maternal circulation and subsequently be transmitted to the fetus. Further analysis revealed that PRV infection disrupts placental vascular architecture and compromises the integrity of tight junction proteins (TJPs) ZO-1 and occludin, facilitating viral entry into fetal tissues. Transcriptomic profiling of placental tissues showed activation of inflammatory responses, oxidative stress, and cell death pathways. Concurrently, genes involved in hormone biosynthesis, angiogenesis, and trophoblast proliferation and differentiation were markedly downregulated. Together, these results indicate that PRV compromises placental integrity in mice through a combination of physical barrier disruption, inflammatory microenvironment formation, and vascular dysfunction. This provides a reference for the mechanism of vertical transmission of PRV through the placenta in mice.

Pseudorabies virus can be transmitted vertically by disrupting the barrier function of the placenta. Maternal viremia drives preferential PRV replication within the placenta. PRV preferentially colonizes decidual and labyrinthine placental regions. PRV can cause pregnancy failure via inflammation.