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Autophagy inhibits viral genome replication and gene expression stages in West Nile virus infection

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Title: Autophagy inhibits viral genome replication and gene expression stages in West Nile virus infection
Authors: Kobayashi, Shintaro Browse this author →KAKEN DB
Orba, Yasuko Browse this author →KAKEN DB
Yamaguchi, Hiroki Browse this author
Takahashi, Kenta Browse this author
Sasaki, Michihito Browse this author →KAKEN DB
Hasebe, Rie Browse this author →KAKEN DB
Kimura, Takashi Browse this author →KAKEN DB
Sawa, Hirofumi Browse this author →KAKEN DB
Keywords: Autophagy
Host defense
Viral replication
Issue Date: 13-Oct-2014
Publisher: Elsevier
Journal Title: Virus Research
Volume: 191
Start Page: 83
End Page: 91
Publisher DOI: 10.1016/j.virusres.2014.07.016
PMID: 25091564
Abstract: Autophagy is a lysosomal degradation pathway that is implicated in many viral infections. However, its role in West Nile virus (WNV) infection remains controversial. In the present study, we examined the relationship between WNV infection and autophagy in infected cells. We demonstrated that LC3-II expression, a molecular marker for autophagosomal membranes, was enhanced in WNV-infected cells 6 h post-infection. LC3-II expression was further enhanced in WNV-inoculated cells when treated with a lysosomal protease inhibitor. Meanwhile, WNV replication in cells lacking Atg5, an essential factor for autophagy, was increased compared with replication in wild-type cells. In addition, WNV replication was inhibited in cells lacking Atg5 when they were transfected with an ATG5 expression plasmid. These results suggest an antiviral role for autophagy in WNV-infected cells. We also examined which viral replication stages were affected by autophagy by using a Tat-beclin 1 peptide to induce autophagy and pseudo-infectious WNV reporter virus particles (WNV-RVPs) that monitor viral genome replication and gene expression stages via GFP expression. We found that autophagy induction in HeLa cells by Tat-beclin 1 peptide 3 h after WNV inoculation inhibited viral replication, and GFP expression was significantly inhibited in wild-type cells when compared with cells lacking Atg5. Taken together, these results suggest that autophagy is induced by WNV infection, and that this induction inhibits WNV replication at the viral genome replication and gene expression stages. (C) 2014 Elsevier B.V. All rights reserved.
Type: article (author version)
Appears in Collections:人獣共通感染症リサーチセンター (Research Center for Zoonosis Control) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小林 進太郎

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