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Activation of Toll‐like receptors inhibits herpes simplex virus‐1 infection of human neuronal cells
Author(s) -
Zhou Yu,
Ye Li,
Wan Qi,
Zhou Lin,
Wang Xu,
Li Jieliang,
Hu Shuxian,
Zhou Dunjin,
Ho Wenzhe
Publication year - 2009
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22110
Subject(s) - innate immune system , tlr3 , interferon , herpes simplex virus , biology , receptor , tlr7 , intracellular , immunity , immune system , virus , toll like receptor , pattern recognition receptor , virology , immunology , microbiology and biotechnology , biochemistry
Toll‐like receptors (TLRs) play an essential role in initiating intracellular type I interferon (IFN)‐mediated innate immunity against viral infections. We examined whether human neuronal cells (primary human neurons, NT2‐N and CHP‐212 cells) express TLRs and mount type I IFN‐mediated innate immunity against herpes simplex virus‐1 (HSV‐1) infection. Human neuronal cells expressed TLR family members 1–10 and IFN‐α/β. The activation of TLR3 or TLR8 by double‐stranded RNA (poly‐I:C) or single‐stranded RNA (ssRNA) induced IFN‐α/β expression. In addition, HSV‐1 infection of human neuronal cells induced IFN‐α expression. Investigation of the mechanisms showed that poly‐I:C or ssRNA treatment enhanced the expression of several IFN regulatory factors. Importantly, the activation of TLR3 or TLR8 by poly‐I:C or ssRNA prior to HSV‐1 infection reduced the susceptibility of the neuronal cells to infection. These observations indicate that human neuronal cells possess intracellular TLR‐mediated innate immune protection against HSV‐1 infection. © 2009 Wiley‐Liss, Inc.