Fibroblast Growth Factor 2 Enhances Zika Virus Infection in Human Fetal Brain.
MAP kinase
Zika virus
astrocytes
congenital
explant
fetal brain
fibroblast growth factor 2
interferon
Journal
The Journal of infectious diseases
ISSN: 1537-6613
Titre abrégé: J Infect Dis
Pays: United States
ID NLM: 0413675
Informations de publication
Date de publication:
13 09 2019
13 09 2019
Historique:
received:
14
12
2018
accepted:
12
02
2019
pubmed:
26
2
2019
medline:
28
5
2020
entrez:
26
2
2019
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 30799482
pii: 5319999
doi: 10.1093/infdis/jiz073
pmc: PMC6743838
doi:
Substances chimiques
Fibroblast Growth Factor 2
103107-01-3
Interferons
9008-11-1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1377-1387Subventions
Organisme : CIHR
ID : PJT-148699
Pays : Canada
Organisme : CIHR
ID : ZV1-149782
Pays : Canada
Informations de copyright
© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.
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