Molecular signatures associated with ZIKV exposure in human cortical neural progenitors

Feiran Zhang(Emory University), Christy Hammack(Florida State University), Sarah C. Ogden(Florida State University), Yichen Cheng(Florida State University), Emily M. Lee(Florida State University), Zhexing Wen(Johns Hopkins Medicine), Xuyu Qian(Johns Hopkins University), Ha Nam Nguyen(Johns Hopkins Medicine), Yujing Li(Emory University), Bing Yao(Emory University), Miao Xu(University of Miami), Tianlei Xu(Emory University), Li Chen(Emory University), Zhiqin Wang(Emory University), Hao Feng(Emory University), Wei-Kai Huang(Johns Hopkins Medicine), Ki‐Jun Yoon(Johns Hopkins University), Chao Shan(The University of Texas Medical Branch at Galveston), Luoxiu Huang(Emory University), Zhaohui Qin(Emory University), Kimberly M. Christian(Johns Hopkins Medicine), Pei‐Yong Shi(The University of Texas Medical Branch at Galveston), Mingjiang Xu(Sylvester Comprehensive Cancer Center), Menghang Xia(National Institutes of Health), Wei Zheng(National Center for Advancing Translational Sciences), Hao Wu(Emory University), Hongjun Song(Johns Hopkins University), Hengli Tang(Florida State University), Guo‐li Ming(Johns Hopkins Medicine), Peng Jin(Emory University)
Nucleic Acids Research
August 31, 2016
Cited by 171Open Access
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Abstract

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 ZIKV C , African ZIKV M , 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, ZIKV C , but not ZIKV M , induces upregulation of viral response genes and TP53. P53 inhibitors can block the apoptosis induced by both ZIKV C and ZIKV M in hNPCs, with higher potency against ZIKV C -induced apoptosis. Our analyses re-veal 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.


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