Since IFN-α/β controls replication and dissemination of many viruses, including other flaviviruses [42]–[46], we reasoned that increased susceptibility of type I IFN-deficient mice to wild-type YFV infection would correspond to higher virus titers and potentially altered tropism compared with 17D-204 virus infection or wild-type YFV infection of disease-resistant WT129 mice. Here, IFNA1 is linked to viral infectious disease.