PT  - JOURNAL ARTICLE
AU  - Feiran Zhang
AU  - Christy Hammack
AU  - Sarah C. Ogden
AU  - Yichen Cheng
AU  - Emily M. Lee
AU  - Zhexing Wen
AU  - Xuyu Qian
AU  - Ha Nam Nguyen
AU  - Yujing Li
AU  - Bing Yao
AU  - Miao Xu
AU  - Tianlei Xu
AU  - Li Chen
AU  - Zhiqin Wang
AU  - Hao Feng
AU  - Wei-Kai Huang
AU  - Ki-jun Yoon
AU  - Chao Shan
AU  - Luoxiu Huang
AU  - Zhaohui Qin
AU  - Kimberly M. Christian
AU  - Pei-Yong Shi
AU  - Mingjiang Xu
AU  - Menghang Xia
AU  - Wei Zheng
AU  - Hao Wu
AU  - Hongjun Song
AU  - Hengli Tang
AU  - Guo-Li Ming
AU  - Peng Jin
TI  - Molecular signatures associated with ZIKV exposure in human cortical neural progenitors
AID  - 10.1101/071183
DP  - 2016 Jan 01
TA  - bioRxiv
PG  - 071183
4099  - http://biorxiv.org/content/early/2016/08/23/071183.short
4100  - http://biorxiv.org/content/early/2016/08/23/071183.full
AB  - Zika virus (ZIKV) infection causes microcephaly and has been linked to other brain abnormalities. How ZIKV impairs brain development and function is unclear. Here we systematically profiled transcriptomes of human neural progenitor cells exposed to Asian ZIKVC, African ZIKVM, and dengue virus (DENV). In contrast to the robust global transcriptome changes induced by DENV, ZIKV has a more selective and larger impact on expression of genes involved in DNA replication and repair. While overall expression profiles are similar, ZIKVC, but not ZIKVM, induces upregulation of viral response genes and TP53. P53 inhibitors can block the apoptosis induced by both ZIKVC and ZIKVM in hNPCs, with higher potency against ZIKVC-induced apoptosis. Our analyses reveal virus- and strain-specific molecular signatures associated with ZIKV infection. These datasets will help to investigate ZIKV-host interactions and identify neurovirulence determinants of ZIKV.