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Intrauterine Zika virus infection of pregnant immunocompetent mice models transplacental transmission and adverse perinatal outcomes

Author

Listed:
  • Meghan S. Vermillion

    (Johns Hopkins Bloomberg School of Public Health
    The Johns Hopkins School of Medicine)

  • Jun Lei

    (Integrated Research Center for Fetal Medicine, Johns Hopkins University School of Medicine)

  • Yahya Shabi

    (Integrated Research Center for Fetal Medicine, Johns Hopkins University School of Medicine)

  • Victoria K. Baxter

    (Johns Hopkins Bloomberg School of Public Health
    The Johns Hopkins School of Medicine)

  • Nathan P. Crilly

    (Johns Hopkins Bloomberg School of Public Health
    Present address: University of Tennessee School of Veterinary Medicine, Knoxville, Tennessee 37996, USA)

  • Michael McLane

    (Integrated Research Center for Fetal Medicine, Johns Hopkins University School of Medicine)

  • Diane E. Griffin

    (Johns Hopkins Bloomberg School of Public Health)

  • Andrew Pekosz

    (Johns Hopkins Bloomberg School of Public Health)

  • Sabra L. Klein

    (Johns Hopkins Bloomberg School of Public Health)

  • Irina Burd

    (Integrated Research Center for Fetal Medicine, Johns Hopkins University School of Medicine)

Abstract

Zika virus (ZIKV) crosses the placenta and causes congenital disease. Here we develop an animal model utilizing direct ZIKV inoculation into the uterine wall of pregnant, immunocompetent mice to evaluate transplacental transmission. Intrauterine inoculation at embryonic day (E) 10, but not E14, with African, Asian or American strains of ZIKV reduces fetal viability and increases infection of placental and fetal tissues. ZIKV inoculation at E10 causes placental inflammation, placental dysfunction and reduces neonatal brain cortical thickness, which is associated with increased activation of microglia. Viral antigen localizes in trophoblast and endothelial cells in the placenta, and endothelial, microglial and neural progenitor cells in the fetal brain. ZIKV infection of the placenta increases production of IFNβ and expression of IFN-stimulated genes 48 h after infection. This mouse model provides a platform for identifying factors at the maternal–fetal interface that contribute to adverse perinatal outcomes in a host with an intact immune system.

Suggested Citation

  • Meghan S. Vermillion & Jun Lei & Yahya Shabi & Victoria K. Baxter & Nathan P. Crilly & Michael McLane & Diane E. Griffin & Andrew Pekosz & Sabra L. Klein & Irina Burd, 2017. "Intrauterine Zika virus infection of pregnant immunocompetent mice models transplacental transmission and adverse perinatal outcomes," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14575
    DOI: 10.1038/ncomms14575
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