ZIKV prevents host mRNA export from the nucleus by disrupting UPF1 function. ZIKV prevents host mRNA export from the nucleus by disrupting UPF1 function

Zika virus (ZIKV) is a mosquito-borne virus that can have dramatic neurodevelopmental consequences when infection occurs in utero. Previous studies demonstrated that ZIKV downregulates the master regulator of nonsense mediated decay, UPF1. To examine whether this process contributes to disruption of neural development, we investigated the effect of ZIKV infection on UPF1 interaction with host RNA in neural progenitor cells. Here, we show that ZIKV-mediated disruption of UPF1 function in neural progenitor cells causes retention of mRNA in the nucleus, resulting in decreased protein levels of specific transcripts involved in neural differentiation. Overall design: UPF1-CLIP Sequencing, RNA Sequencing and Fractionated RNA sequencing comparing Mock and ZIKV-infected Neural progenitor cells