New research from the Gale lab reveals that maternal to fetal prenatal exposure to Zika virus leads to profound disruption of fetal myelin, myelin unwrapping from neurons, and extensive suppression in gene expression for key components of oligodendrocyte maturation and myelin production. Because myelin is critical for cortical development, Zika virus-related perturbations in fetal brain myelination could render long-term consequences on childhood neurodevelopment resulting from Zika virus infection during pregnancy.