Type I interferons instigate fetal demise after Zika virus infection.

ABSTRACT: Zika virus (ZIKV) infection during pregnancy is associated with adverse fetal outcomes, including microcephaly, growth restriction, and fetal demise. Type I interferons (IFNs) are essential for host resistance against ZIKV, and IFN-α/β receptor (IFNAR)-deficient mice are highly susceptible to ZIKV infection. Severe fetal growth restriction with placental damage and fetal resorption is observed after ZIKV infection of type I IFN receptor knockout (Ifnar1^-/-) dams mated with wild-type sires, resulting in fetuses with functional type I IFN signaling. The role of type I IFNs in limiting or mediating ZIKV disease within this congenital infection model remains unknown. In this study, we challenged Ifnar1^-/- dams mated with Ifnar1^+/- sires wit

SUBMITTER: Yockey LJ 

PROVIDER: S-EPMC6049088 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature