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Dengue virus infection increases microglial cell migration
- Source :
- Scientific Reports, Vol 7, Iss 1, Pp 1-11 (2017), Scientific Reports
- Publication Year :
- 2017
- Publisher :
- Nature Portfolio, 2017.
-
Abstract
- Activated microglial cells are present in dengue virus (DENV)-infected brains; however, the possible effects of DENV on microglia remain unclear. Here, we demonstrated DENV caused infection, including viral entry, RNA replication, viral protein expression, and virus release, in the murine microglial cell line BV2. DENV infection caused an increase in the formation of the multipolar phenotype in vitro and in vivo without affecting cell growth and cytotoxicity. DENV infection considerably increased cell motility and disrupting either actin filaments or clathrin retarded such effect. Increase in cell migration was only occurred by DENV infection following a clathrin-regulated endocytosis of DENV entry. Ultraviolet-inactivated DENV did not affect cell migration, and pharmacologically blocking toll-like receptor (TLR) 3 and TLR3-related signaling pathways reduced the DENV-induced increase in cell migration. These results demonstrate an advanced effect of DENV infection on microglial migration via a mechanism involving viral entry, RNA release, and TLR3 signal activation.
- Subjects :
- 0301 basic medicine
viruses
Science
Dengue virus
Biology
medicine.disease_cause
Virus Replication
Models, Biological
Article
Cell Line
Dengue
03 medical and health sciences
Mice
0302 clinical medicine
Viral entry
Cell Movement
medicine
Animals
Humans
Multidisciplinary
Cell growth
virus diseases
Cell migration
Dengue Virus
Virus Internalization
biochemical phenomena, metabolism, and nutrition
Actin cytoskeleton
Virology
Virus Release
Clathrin
Endocytosis
Toll-Like Receptor 3
Microglial cell migration
Actin Cytoskeleton
030104 developmental biology
Viral replication
RNA, Viral
Medicine
Microglia
030215 immunology
Signal Transduction
Subjects
Details
- Language :
- English
- ISSN :
- 20452322
- Volume :
- 7
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Scientific Reports
- Accession number :
- edsair.doi.dedup.....4308650f6625ac33853beb7d26a47988