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

The interferon boomerang

Interferon-α/β receptor (IFNAR)–deficient mice are highly susceptible to viruses, including Zika virus (ZIKV). Previous studies modeled ZIKV infection during pregnancy in mice by crossing Ifnar1−/− females to wild-type males, generating Ifnar1+/− fetuses that retain type I interferon (IFN) responsiveness. Yockey et al. have directly examined the role of fetal type I IFN signaling in protection in this context, by crossing Ifnar1−/− females to Ifnar1+/− males. Although Ifnar1−/− fetuses had higher ZIKV titers as compared with Ifnar1+/− fetuses, Ifnar1−/− fetuses survived longer. Furthermore, they found that activation of type I IFN signaling in the placentas of Ifnar1+/− fetuses led to fetal hypoxia, demise, and resorption. Beyond ZIKV infection, the study calls for closer examination of the role of IFNs in pregnancy-associated complications.

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