Zika virus (ZIKV) infection during pregnancy is associated with adverse fetal outcomes including microcephaly, growth restriction, and fetal demise. While ZIKV is primarily transmitted by the mosquito, Aedes Aegypti, it can also be sexually transmitted. Type I interferons (IFNs) are essential for host resistance against ZIKV, and most mouse models of ZIKV infection require attenuation of the IFN-α/β receptor (IFNAR) signaling pathway. Severe fetal growth restriction with placental damage or fetal resorption have been demonstrated after infection of type I IFN receptor knockout (Ifnar1-/-) females mice crossed to wild-type males. Within this context, all fetuses have functional type I IFN signaling, as they are Ifnar1 heterozygotes (Ifnar1+/-). In order to investigate the role of IFNAR in controlling ZIKV infection and disease in the developing fetus, we challenged Ifnar1-/- dams mated with Ifnar1+/- sires, resulting in pregnant dams that carry a mixture of fetuses that either expressed IFNAR (Ifnar1+/-) or did not (Ifnar1-/-) within the same uterus. Unexpectedly, we found that only Ifnar1+/- fetuses were resorbed after ZIKV infection during early pregnancy, whereas their Ifnar1-/- littermates continue to develop normally. Analyses of the fetus and placenta revealed that type I IFNs inhibit proper development of the placental labyrinth. Our results implicate type I IFNs as a possible mediator of pregnancy complications, including spontaneous abortions and growth restrictions in the context of viral infections.