This antagonism of the type I IFN receptor (Ifnar) signaling in a species-specific manner by ZIKV explains the more severe pathogenesis of ZIKV infection in mice with immature or compromised immune systems compared to adult immunocompetent mice, and why disruption of the Ifnar1 signaling increases susceptibility of mice to lethal ZIKV infection. This evidence concerns the gene IFNAR1 and Zika virus infectious disease.