期刊
CELL HOST & MICROBE
卷 22, 期 3, 页码 366-+出版社
CELL PRESS
DOI: 10.1016/j.chom.2017.08.012
关键词
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资金
- NIH [R01 AI073755, R01 AI104972, U19 AI083019, R01 HD091218, T32 AI007172, R01 HD075665]
- Burroughs Wellcome Investigators in the Pathogenesis of Infectious Disease Award
- [P30CA047904]
Although Zika virus (ZIKV)-induced congenital disease occurs more frequently during early stages of pregnancy, its basis remains undefined. Using established type I interferon (IFN)-deficient mouse models of ZIKV transmission in utero, we found that the placenta and fetus were more susceptible to ZIKV infection at earlier gestational stages. Whereas ZIKV infection at embryonic day 6 (E6) resulted in placental insufficiency and fetal demise, infections at midstage (E9) resulted in reduced cranial dimensions, and infection later in pregnancy (E12) caused no apparent fetal disease. In addition, we found that fetuses lacking type III IFN-lambda signaling had increased ZIKV replication in the placenta and fetus when infected at E12, and reciprocally, treatment of pregnant mice with IFN-lambda 2 reduced ZIKV infection. IFN-l treatment analogously diminished ZIKV infection in human midgestation fetal-and maternal-derived tissue explants. Our data establish a model of gestational stage dependence of ZIKV pathogenesis and IFN-lambda-mediated immunity at the maternal-fetal interface.
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