Some children with proven intrauterine Zika virus (ZIKV) infection who were born asymptomatic subsequently manifested neurodevelopmental delays.

Our data, using an in vivo model of prenatal infection, demonstrates a vulnerability of early myelinating oligodendrocytes (see Fig. 4 from our manuscript below, showing evidence that oligodendrocytes are dying following ZIKV infection). Could myelin deficits explain transient neurodevelopmental delays?