Transcriptional analysis of ZIKV-infected Ifnar-/- and Ifnar+/- placentas and IFN-beta (IFN-b) or IFN-lambda (IFN-l) treated human mid-gestation chorionic villus explants
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ABSTRACT:
ORGANISM(S): Mus musculus Homo sapiens
PROVIDER: GSE104349 | GEO | 2017/12/31
SECONDARY ACCESSION(S): PRJNA412399
REPOSITORIES: GEO
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Project description:Purpose: Treatment of midgestation chorionic villus explants with recombinant IFN-b leads to morphological changes including formation of syncitial knots. However, treatment of explants with IFN-l, which is constitutively expressed by syncytiotrophoblasts, is not sufficient to cause these same changes. To understand the different transcriptional changes induced by IFN-b and IFN-l and underlying cause of these morphological changes, we performed RNAsequencing after these different treatments. Methods: Chorionic villi of 18-21 gestation week placentas were dissected. Explants were cultured in DMEM F/12 with 1000 U recombinant IFN-b or 1000U recombinant IFN-l for 24 hours. RNA was then isolated from explants, and RNAsequencing was performed to assess transcriptional changes. Results/ Conclusions: IFN-b but not IFN-l induces interferon stimulated genes (ISGs) in mid gestation chorionic villus explants.
2017-12-31 | GSE104348 | GEO
Project description:Transcriptional analysis of ZIKV-infected Ifnar-/- and Ifnar+/- placentas and IFN-beta (IFN-b) or IFN-lambda (IFN-l) treated human mid-gestation chorionic villus explants
| PRJNA412399 | ENA
Project description:Analysis of transcriptional differences after IFN-beta (IFN-b) or IFN-lambda (IFN-l) treated human mid-gestation chorionic villus explants
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Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.
2017-12-31 | GSE98423 | GEO
Project description: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-λ signaling had increased ZIKV replication in the placenta and fetus when infected at E12, and reciprocally, treatment of pregnant mice with IFN-λ2 reduced ZIKV infection. IFN-λ 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-λ-mediated immunity at the maternal-fetal interface.
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Project description:Zika virus infection can result in devastating pregnancy outcomes when it crosses the placental barrier. For human pregnancies, the mechanisms of vertical transmission remain enigmatic. Utilizing a human placenta-cotyledon perfusion model, we examined Zika virus exposure in the absence of maternal factors. To distinguish responses related to viral infection vs. recognition, we evaluated cotyledons perfused with either active or inactivated Zika virus. Active Zika virus exposure resulted in infection, cell death and syncytium injury. Pathology corresponded with transcriptional changes related to inflammation and innate immunity. Inactive Zika virus exposure also led to syncytium injury and related changes in gene expression but not cell death. Our observations reveal pathologies and innate immune responses that are dependent on infection or virus placenta interactions independent of productive infection. Importantly, our findings indicate that Zika virus can infect and compromise placentas in the absence of maternal humoral factors that may be protective.
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