Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 220, Issue 8, Pages 1377-1387Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/infdis/jiz073
Keywords
Zika virus; fibroblast growth factor 2; astrocytes; fetal brain; explant; interferon; congenital; MAP kinase
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Funding
- Canadian Institutes of Health Research [PJT-148699, ZV1149782]
- Women and Children's Health Research Institute
- Li Ka Shing Institute of Virology
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Zika virus (ZIKV) is an emerging pathogen that can cause microcephaly and other neurological defects in developing fetuses. The cellular response to ZIKV in the fetal brain is not well understood. Here, we show that ZIKV infection of human fetal astrocytes (HFAs), the most abundant cell type in the brain, results in elevated expression and secretion of fibroblast growth factor 2 (FGF2). This cytokine was shown to enhance replication and spread of ZIKV in HFAs and human fetal brain explants. The proviral effect of FGF2 is likely mediated in part by suppression of the interferon response, which would represent a novel mechanism by which viruses antagonize host antiviral defenses. We posit that FGF2-enhanced virus replication in the fetal brain contributes to the neurodevelopmental disorders associated with in utero ZIKV infection. As such, targeting FGF2-dependent signaling should be explored further as a strategy to limit replication of ZIKV.
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