| Literature DB >> 27180225 |
Jonathan J Miner1, Bin Cao2, Jennifer Govero1, Amber M Smith1, Estefania Fernandez3, Omar H Cabrera4, Charise Garber1, Michelle Noll1, Robyn S Klein5, Kevin K Noguchi4, Indira U Mysorekar6, Michael S Diamond7.
Abstract
Zika virus (ZIKV) infection in pregnant women causes intrauterine growth restriction, spontaneous abortion, and microcephaly. Here, we describe two mouse models of placental and fetal disease associated with in utero transmission of ZIKV. Female mice lacking type I interferon signaling (Ifnar1(-/-)) crossed to wild-type (WT) males produced heterozygous fetuses resembling the immune status of human fetuses. Maternal inoculation at embryonic day 6.5 (E6.5) or E7.5 resulted in fetal demise that was associated with ZIKV infection of the placenta and fetal brain. We identified ZIKV within trophoblasts of the maternal and fetal placenta, consistent with a trans-placental infection route. Antibody blockade of Ifnar1 signaling in WT pregnant mice enhanced ZIKV trans-placental infection although it did not result in fetal death. These models will facilitate the study of ZIKV pathogenesis, in utero transmission, and testing of therapies and vaccines to prevent congenital malformations.Entities:
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Year: 2016 PMID： 27180225 PMCID： PMC4874881 DOI： 10.1016/j.cell.2016.05.008
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582