| First Author | Jagger BW | Year | 2017 |
| Journal | Cell Host Microbe | Volume | 22 |
| Issue | 3 | Pages | 366-376.e3 |
| PubMed ID | 28910635 | Mgi Jnum | J:272653 |
| Mgi Id | MGI:6285006 | Doi | 10.1016/j.chom.2017.08.012 |
| Citation | Jagger BW, et al. (2017) Gestational Stage and IFN-lambda Signaling Regulate ZIKV Infection In Utero. Cell Host Microbe 22(3):366-376.e3 |
| abstractText | 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-lambda2 reduced ZIKV infection. IFN-lambda 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. |
