We therefore hypothesize that in addition to mediating the effects of putative entry receptors on host cells being a key ZIKV infection mechanism, the ability of ZIKV to defeat the host IFN system, possibly through expressing multiple viral factors that interfere with multiple steps and nodes along the IFN signaling cascade, may also represent a key contributor to its broad cellular tropism and intracellular persistence. The gene discussed is IFNA1; the disease is Zika virus infectious disease.