Molecular signatures associated with ZIKV exposure in human cortical neural progenitors

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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 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 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.
Publisher
OXFORD UNIV PRESS
Issue Date
2016-10
Language
English
Article Type
Article
Citation

NUCLEIC ACIDS RESEARCH, v.44, no.18, pp.8610 - 8620

ISSN
0305-1048
DOI
10.1093/nar/gkw765
URI
http://hdl.handle.net/10203/246057
Appears in Collection
BS-Journal Papers(저널논문)
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