As ZIKV infections have been associated with increasing rates of GBS and other neurological disorders, IFNAR-deficient models on a C57BL/6 background have demonstrated ZIKV dissemination to the CNS, accompanied by neurological deficits, and can be useful for studying the mechanism of ZIKV-induced neuropathology [16,18,30,31]. This evidence concerns the gene IFNAR1 and Zika virus infectious disease.