The critical role of the IFN-I response in controlling ZIKV infection is supported by the fact that Ifnar1−/− mice lacking IFN-α/β receptor and Irf3−/− Irf5−/− Irf7−/− triple knockout mice, which don’t produce IFN-α/ß, are highly vulnerable to ZIKV and more likely to develop signs of neurological disease associated with high viral load in the brain and to die within 1 week of infection compared to immunocompetent WT mice (7). This evidence concerns the gene IFNA1 and infection.