Open AccessDengue virus infection increases microglial cell migration
Author(s) -
Ming Kai Jhan,
Tsung-Cheng Tsai,
ChienChin Chen,
ChengChieh Tsai,
Yi Lin Cheng,
Yi Chao Lee,
Chiung Yuan Ko,
Yee Shin Lin,
Chih Peng Chang,
Liang Lin,
Chiou Feng Lin
Publication year - 2017
Publication title -
scientific reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.24
H-Index - 213
ISSN - 2045-2322
DOI - 10.1038/s41598-017-00182-z
Subject(s) - dengue virus , biology , viral replication , tlr3 , microbiology and biotechnology , viral entry , virology , cell migration , cell culture , microglia , cell , endocytosis , virus , toll like receptor , innate immune system , immunology , inflammation , immune system , genetics
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.