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. Ultravioletinactivated 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.
Original language | English |
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Article number | 91 |
Journal | Scientific Reports |
Volume | 7 |
Issue number | 1 |
DOIs | |
Publication status | Published - Jan 1 2017 |
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ASJC Scopus subject areas
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Cite this
Dengue virus infection increases microglial cell migration. / Jhan, Ming Kai; Tsai, Tsung Ting; Chen, Chia Ling; Tsai, Cheng Chieh; Cheng, Yi Lin; Lee, Yi Chao; Ko, Chiung Yuan; Lin, Yee Shin; Chang, Chih Peng; Lin, Liang Tzung; Lin, Chiou Feng.
In: Scientific Reports, Vol. 7, No. 1, 91, 01.01.2017.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Dengue virus infection increases microglial cell migration
AU - Jhan, Ming Kai
AU - Tsai, Tsung Ting
AU - Chen, Chia Ling
AU - Tsai, Cheng Chieh
AU - Cheng, Yi Lin
AU - Lee, Yi Chao
AU - Ko, Chiung Yuan
AU - Lin, Yee Shin
AU - Chang, Chih Peng
AU - Lin, Liang Tzung
AU - Lin, Chiou Feng
PY - 2017/1/1
Y1 - 2017/1/1
N2 - 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. Ultravioletinactivated 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.
AB - 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. Ultravioletinactivated 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=85030844225&partnerID=8YFLogxK
U2 - 10.1038/s41598-017-00182-z
DO - 10.1038/s41598-017-00182-z
M3 - Article
AN - SCOPUS:85030844225
VL - 7
JO - Scientific Reports
JF - Scientific Reports
SN - 2045-2322
IS - 1
M1 - 91
ER -