Attenuated neurogenesis in late fetal neurogenic zones accompanied by granule neuron dysmorphia in the dentate gyrus after maternal ZIKV infection. (A–C) Adjacent sections were labeled for Sox2+ NSCs (left sections) and Tbr2+ IPs (right sections) by immunohistochemistry (brown, Tbr2 is also known as Eomes) and quantified by image analysis (D, E). Fetal Sox2+ NSCs were significantly reduced in the SVZ and disorganized in the subgranular zone (SGZ) with congenital ZIKV exposure. In the SGZ, there was a significant and marked reduction in Tbr2+ IPs in ZIKA fetuses compared to controls. Asterisks indicate disordered NSC in the SGZ neurogenic niche. Arrows indicate a loss of continuity in the granule zone. (F–H) Confocal microscopy to identify NSCs (Sox2+, red), IPs (Tbr2+, green) and immature granule neurons (Dcx, doublecortin, white; Dapi nuclei, blue) in adjacent sections revealed disordered NSCs in the SGZ niche, loss of neurogenic output (Tbr2+ IPs), and dysmorphic granule neurons with congenital ZIKV exposure. Data shown as mean ± standard deviation of either Sox2+ or Tbr2+ cell counts per mm2 (**p<0.01).