Journal
CELL HOST & MICROBE
Volume 20, Issue 4, Pages 423-428Publisher
CELL PRESS
DOI: 10.1016/j.chom.2016.09.006
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Funding
- Tasha and John Morgridge Endowed Faculty Scholar (C.A.B.) in Pediatric Translational Medicine from Stanford Child Health Research Institute and Stanford University School of Medicine, NIH Director's New Innovator Award [1DP2AI112193]
- NIDCR U01 [DE024430]
- March of Dimes Birth Defects Foundation
- Howard Hughes Medical Institute
- NIDCR [1F31DE025534]
- Stanford Graduate Fellowship
- NICHD [1F31HD089675]
- Stanford Systems Biology Seed Grant
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Zika virus (ZIKV) infection during pregnancy is linked to microcephaly, which is attributed to infection of developing brain structures. ZIKV infects neural progenitor cells in vitro, though its effects on other developmentally relevant stem cell populations, including cranial neural crest cells (CNCCs), have not been assessed. CNCCs give rise to most cranial bones and exert paracrine effects on the developing brain. Here, we report that CNCCs are productively infected by ZIKV, but not by the related dengue virus. ZIKV-infected CNCCs undergo limited apoptosis but secrete cytokines that promote death and drive aberrant differentiation of neural progenitor cultures. Addition of two such cytokines, LIF or VEGF, at levels comparable to those secreted by ZIKV-infected CNCCs is sufficient to recapitulate premature neuronal differentiation and apoptotic death of neural progenitors. Thus, our results suggest that CNCC infection by ZIKV may contribute to associated embryopathies through signaling crosstalk between developing face and brain structures.
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