Research ArticleANTIVIRAL IMMUNITY

Type I interferons instigate fetal demise after Zika virus infection

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Science Immunology  05 Jan 2018:
Vol. 3, Issue 19, eaao1680
DOI: 10.1126/sciimmunol.aao1680

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  • RE: Type I interferons instigate fetal demise after Zika virus infection
    • Dr Dianne Sika-Paotonu, Associate Dean (Pacific)/Senior Lecturer Pathology & Molecular Medicine, Wellington School of Medicine & Health Sciences, University of Otago, New Zealand

    To the Editor,

    I read with keen interest the article authored by Yockey L.J. et al (1) and entitled: “Type 1 interferons instigate fetal demise after Zika virus infection.”

    This series of experiments sought to improve understanding of the role of Type 1 IFN’s during pregnancy complications and Zika virus (ZIKV) infection.

    This work showed that Type 1 IFN’s were needed to resist ZIKV infection.
    A mouse model of ZIKV infection was employed that crossed lfnar-/- dams with lfnar+/- sires to generate pregnant mothers carrying foetuses that were either lfnar-/- or lfnar+/- within same litter.

    After ZIKV infection, fetuses that were lfnar-/- displayed higher viral titers in their placentas than lfna+/- foetuses. Early infection with ZIKV during pregnancy resulted in reabsorption of the lfna+/- foetuses only, with lfna-/- foetuses continuing on to develop. Type 1 IFN signalling in the lfna+/- placentas was also shown to link with fetal hypoxia, demise and fetal reabsorption.

    Further experiments showed that Type 1 IFN signalling post ZIKV infection, inhibited development of the placental labyrinth causing abnormal architecture of the maternal-fetal barrier. Importantly, ZIKV infection during later pregnancy resulted in placental morphology that was modified, causing cytoskeletal rearrangements.

    Points of interest include the implication of Type 1 IFN’s as a possible type of control mechanism and potential mediator in pregnancy comp...

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    Competing Interests: None declared.

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