The 2015 Zika virus (ZIKV) outbreak caused global concern when it was determined to cause microcephaly, hearing loss, and other neurodevelopmental manifestations upon fetal exposure. Significant progress has been made in our understanding of the interactions between ZIKV and the pregnant host, but there is still a critical need to understand how ZIKV and other neurotropic viruses affect fetal neurodevelopment. Diaphanous-related formins (Diaphs) have recently been identified as microcephaly-associated proteins in humans and mice. Mutations in Diaphs affect the function of neural progenitor cells, much like prenatal viral infection. We present a novel hypothesis that viruses ‘hijack’ Diaphs in neural progenitor cells, causing autonomous differentiation and apoptosis of neural progenitor cells, which could potentially contribute to virus-associated neurological pathologies.

当2015年寨卡病毒（ZIKV）爆发被确定导致胎儿暴露于小头畸形，听力下降和其他神经发育表现时，引起了全球关注。在我们对ZIKV与怀孕宿主之间相互作用的理解上已经取得了重大进展，但是仍然迫切需要了解ZIKV和其他嗜神经病毒如何影响胎儿神经发育。最近，透照相关的formins（Diaphs）被鉴定为人类和小鼠中与小头畸形相关的蛋白。膜上的突变会影响神经祖细胞的功能，就像产前病毒感染一样。我们提出了一个新的假设，即病毒会“劫持”神经祖细胞中的膜，导致神经祖细胞的自主分化和凋亡，