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

Meghan S. Vermillion, Jun Lei, Yahya Shabi, Victoria K. Baxter, Nathan P. Crilly, Michael McLane, Diane E. Griffin, Andrew Pekosz, Sabra L. Klein () and Irina Burd ()
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Meghan S. Vermillion: Johns Hopkins Bloomberg School of Public Health
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
Nathan P. Crilly: Johns Hopkins Bloomberg School of Public Health
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

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: 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.

Date: 2017
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DOI: 10.1038/ncomms14575

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