Journal
NUCLEIC ACIDS RESEARCH
Volume 44, Issue 18, Pages 8610-8620Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkw765
Keywords
-
Categories
Funding
- National Institutes of Health (NIH) [AI119530, AI111250, NS048271, NS095348, NS047344, MH087874, NS079625]
- Maryland Stem Cell Research Fund
- start-up fund
- College of Arts and Sciences and Department of Biological Science at Florida State University seed fund
- Emory Genetics Discovery Fund
- Emory Integrated Genomics Core (EIGC)
- Emory University School of Medicine
- National Center for Advancing Translational Sciences of the National Institutes of Health [UL1TR000454]
- NIH
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available