Zika virus differentially infects human neural progenitor cells according to their state of differentiation and dysregulates neurogenesis through the Notch pathway
by Ferraris et al.Results from this research show that the differentiation state of hNPCs is a significant factor contributing to the outcome of ZIKV infection and furthermore suggest that ZIKV infection might initiate early activation of the Notch pathway resulting in an abnormal differentiation process, implicated in ZIKV-induced brain injury.
Stress-induced unfolded protein response contributes to Zika virus–associated microcephaly
by Gladwyn-Ng et al.In order to understand the mechanism of Zika virus-associated microcephaly, the authors combined analysis of human fetuses infected with Zika virus, cultures of human neuronal stem cells and mice embryos. They showed that ZIKV infection of cortical progenitors controlling neurogenesis triggers a stress in the endoplasmic reticulum in the embryonic brain, inducing signals in response to incorrect protein con-formation.