IFNAR2 and Zika virus infectious disease: Upon infection with ZIKVFP and ZIKVMP we observed the same phenotypes in iPS-MGL that were previously seen in IFNAR2-deficient iPS-Mφ, including a robust pro-inflammatory response, significantly heightened ZIKV replication, increased infectious particle release and vulnerability to CPE (Figures 9B–E), indicating that IFN-I mediated restraint of ZIKV replication and cytopathicity is also key to the response of CNS-resident human microglia to ZIKV infection.