Framing our results in this comparative context suggests that mild ZIKV infection during human mid-gestation could perturb NPC and FGN programs during a critical window for cortical and hippocampal circuit assembly, with consequences that manifest later in childhood and adolescence as altered excitability and spontaneous behavioral structure, even in the absence of overt structural malformations at birth. This evidence concerns the gene NPC1 and Zika virus infectious disease.