Zika virus (ZIKV) infection results in embryonic microcephaly and has been declared a global health emergency by the World Health Organization. Disruption of the neural progenitor cells is considered to be the major cause of microcephaly; however, the fate of other cell types, including differentiated neurons and vascular cells, remains unknown. Since infected mouse embryos die perinatally, it also remains unknown whether ZIKV infection can cause postnatal microcephaly in animal models. Now, on p. 4127, Jian-Fu Chen and colleagues report a postnatal model for ZIKV infection using intracerebral inoculation of embryonic brains with the ZIKV. The infected pups survive after birth and show postnatal microcephaly, which bears relevance for a better understanding of the microcephaly observed in ZIKV-infected newborn humans. In addition to microcephaly, the postnatal mouse model recapitulates several aspects of fetal brain abnormalities associated with ZIKV in humans, including extensive neuronal apoptosis and loss, axonal rarefaction, corpus callosum diminishment, and reactive astrocyte and microglial cell accumulation. Furthermore, the authors show that ZIKV infection leads to increased vessel density and vessel diameter, and causes blood–brain barrier leakage in the developing brain. While further research is required to better characterise the approach, the development of a postnatal model for ZIKV infection is an important step forward in understanding this disease, and the findings reported by the authors offer novel insight into the pathology of ZIKV infection in the postnatal setting.
