RT Journal Article
SR Electronic
T1 Molecular signatures associated with ZIKV exposure in human cortical neural progenitors
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 071183
DO 10.1101/071183
A1 Feiran Zhang
A1 Christy Hammack
A1 Sarah C. Ogden
A1 Yichen Cheng
A1 Emily M. Lee
A1 Zhexing Wen
A1 Xuyu Qian
A1 Ha Nam Nguyen
A1 Yujing Li
A1 Bing Yao
A1 Miao Xu
A1 Tianlei Xu
A1 Li Chen
A1 Zhiqin Wang
A1 Hao Feng
A1 Wei-Kai Huang
A1 Ki-jun Yoon
A1 Chao Shan
A1 Luoxiu Huang
A1 Zhaohui Qin
A1 Kimberly M. Christian
A1 Pei-Yong Shi
A1 Mingjiang Xu
A1 Menghang Xia
A1 Wei Zheng
A1 Hao Wu
A1 Hongjun Song
A1 Hengli Tang
A1 Guo-Li Ming
A1 Peng Jin
YR 2016
UL http://biorxiv.org/content/early/2016/08/23/071183.abstract
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.