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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? https://onlinelibrary.wiley.com/doi/epdf/10.1002/glia.24010