IFNG and Zika virus infectious disease: WNV and ZIKV infection of these mice followed by tamoxifen injection showed that, upon sensing of T-cell-derived Ifn-γ, CX3CR1+ cells such microglia potentiated spatial-learning defects after viral clearance.36 In the viral déjà vu model, T-cell-derived Ifn-γ also played a pathological role, but in contrast to direct stimulation of microglia, in the viral déjà vu model, Ifn-γ stimulation of neurons led to Ccl2 production in the neurons, which mediated phagocyte recruitment to these neurons.47