Therefore, unlike earlier studies all performed in IFNAR deficient mice (22–24), in which the increased viral load in the CNS could represent a consequence of augmented viral spread from peripheral sites, our results obtained in WT mice clearly demonstrate that the reduced viral replication in the CNS reflects in situ antiviral activity since there is no detectable peripheral ZIKV infection in WTs. Here, IFNAR1 is linked to Zika virus infectious disease.