The causal link between Zika virus (
ZIKV) infection and
microcephaly has raised alarm worldwide. Microglial
hyperplasia, reactive
gliosis, and myelination delay have been reported in ZIKV-infected microcephalic fetuses. However, whether and how
ZIKV infection affects glial cell development remain unclear. Here we show that
ZIKV infection of embryos at the later stage of development causes severe
microcephaly after birth. ZIKV infects the glial progenitors during brain development. Specifically,
ZIKV infection disturbs the proliferation and differentiation of the oligodendrocyte progenitor cells and leads to the abolishment of oligodendrocyte development. More importantly, a single
intraperitoneal injection of pregnant mice with a human monoclonal
neutralizing antibody provides full protection against
ZIKV infection and its associated damages in the developing fetuses. Our results not only provide more insights into the pathogenesis of
ZIKV infection, but also present a new model for the preclinical test of prophylactic and therapeutic agents against
ZIKV infection.