Journal
CELL
Volume 165, Issue 5, Pages 1080-1090Publisher
CELL PRESS
DOI: 10.1016/j.cell.2016.05.008
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Funding
- NIH [R01 AI073755, R01 AI104972, R01 HD052664, R01 NS052632]
- Intellectual and Developmental Disabilities Research Center at Washington University (NIH/NICHD) [U54 HD087011]
- Rheumatology Research Foundation Scientist Development Award
- NIH Pre-doctoral training grant award [T32 AI007163]
- NIH Research Education Program [R25 HG006687]
- Preventing Prematurity Initiative grant from the Burroughs Wellcome Fund
- Prematurity Research Initiative Investigator award from the March of Dimes
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Zika virus (ZIKV) infection in pregnant women causes intrauterine growth restriction, spontaneous abortion, and microcephaly. Here, wedescribe 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 transplacental 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.
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