Autophagic machinery activated by dengue virus enhances virus replication

Ying Ray Lee; Huan Yao Lei; Ming Tao Liu; Jen Ren Wang; Shun Hua Chen; Ya Fen Jiang-Shieh; Yee Shin Lin; Trai Ming Yeh; Ching Chuan Liu; Hsiao Sheng Liu

doi:10.1016/j.virol.2008.02.016

Autophagic machinery activated by dengue virus enhances virus replication

Ying Ray Lee, Huan Yao Lei, Ming Tao Liu, Jen Ren Wang, Shun Hua Chen, Ya Fen Jiang-Shieh, Yee Shin Lin, Trai Ming Yeh, Ching Chuan Liu, Hsiao Sheng Liu

Research output: Contribution to journal › Article › peer-review

249 Citations (Scopus)

Abstract

Autophagy is a cellular response against stresses which include the infection of viruses and bacteria. We unravel that Dengue virus-2 (DV2) can trigger autophagic process in various infected cell lines demonstrated by GFP-LC3 dot formation and increased LC3-II formation. Autophagosome formation was also observed under the transmission electron microscope. DV2-induced autophagy further enhances the titers of extracellular and intracellular viruses indicating that autophagy can promote viral replication in the infected cells. Moreover, our data show that ATG5 protein is required to execute DV2-induced autophagy. All together, we are the first to demonstrate that DV can activate autophagic machinery that is favorable for viral replication.

Original language	English
Pages (from-to)	240-248
Number of pages	9
Journal	Virology
Volume	374
Issue number	2
DOIs	https://doi.org/10.1016/j.virol.2008.02.016
Publication status	Published - 2008 May 10

All Science Journal Classification (ASJC) codes

Virology

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@article{f456876963ca48be94650a2b75ef18f8,

title = "Autophagic machinery activated by dengue virus enhances virus replication",

abstract = "Autophagy is a cellular response against stresses which include the infection of viruses and bacteria. We unravel that Dengue virus-2 (DV2) can trigger autophagic process in various infected cell lines demonstrated by GFP-LC3 dot formation and increased LC3-II formation. Autophagosome formation was also observed under the transmission electron microscope. DV2-induced autophagy further enhances the titers of extracellular and intracellular viruses indicating that autophagy can promote viral replication in the infected cells. Moreover, our data show that ATG5 protein is required to execute DV2-induced autophagy. All together, we are the first to demonstrate that DV can activate autophagic machinery that is favorable for viral replication.",

author = "Lee, {Ying Ray} and Lei, {Huan Yao} and Liu, {Ming Tao} and Wang, {Jen Ren} and Chen, {Shun Hua} and Jiang-Shieh, {Ya Fen} and Lin, {Yee Shin} and Yeh, {Trai Ming} and Liu, {Ching Chuan} and Liu, {Hsiao Sheng}",

note = "Funding Information: We thank Dr. N. Mizushima and Dr. T. Yoshimori for providing the GFP-LC3 plasmid and ATG5 wild-type as well as ATG5 knockout MEF cells. This research was supported by grants NHRI-CN-CL9303P, NHRI-CN-CL9601S from the National Health Research Institute, and NSC 96-2628-B-006-003-MY3 from National Science Council, Taiwan, R.O.C. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.",

year = "2008",

month = may,

day = "10",

doi = "10.1016/j.virol.2008.02.016",

language = "English",

volume = "374",

pages = "240--248",

journal = "Virology",

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publisher = "Academic Press Inc.",

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T1 - Autophagic machinery activated by dengue virus enhances virus replication

AU - Lee, Ying Ray

AU - Lei, Huan Yao

AU - Liu, Ming Tao

AU - Wang, Jen Ren

AU - Chen, Shun Hua

AU - Jiang-Shieh, Ya Fen

AU - Lin, Yee Shin

AU - Yeh, Trai Ming

AU - Liu, Ching Chuan

AU - Liu, Hsiao Sheng

N1 - Funding Information: We thank Dr. N. Mizushima and Dr. T. Yoshimori for providing the GFP-LC3 plasmid and ATG5 wild-type as well as ATG5 knockout MEF cells. This research was supported by grants NHRI-CN-CL9303P, NHRI-CN-CL9601S from the National Health Research Institute, and NSC 96-2628-B-006-003-MY3 from National Science Council, Taiwan, R.O.C. Copyright: Copyright 2008 Elsevier B.V., All rights reserved.

PY - 2008/5/10

Y1 - 2008/5/10

N2 - Autophagy is a cellular response against stresses which include the infection of viruses and bacteria. We unravel that Dengue virus-2 (DV2) can trigger autophagic process in various infected cell lines demonstrated by GFP-LC3 dot formation and increased LC3-II formation. Autophagosome formation was also observed under the transmission electron microscope. DV2-induced autophagy further enhances the titers of extracellular and intracellular viruses indicating that autophagy can promote viral replication in the infected cells. Moreover, our data show that ATG5 protein is required to execute DV2-induced autophagy. All together, we are the first to demonstrate that DV can activate autophagic machinery that is favorable for viral replication.

AB - Autophagy is a cellular response against stresses which include the infection of viruses and bacteria. We unravel that Dengue virus-2 (DV2) can trigger autophagic process in various infected cell lines demonstrated by GFP-LC3 dot formation and increased LC3-II formation. Autophagosome formation was also observed under the transmission electron microscope. DV2-induced autophagy further enhances the titers of extracellular and intracellular viruses indicating that autophagy can promote viral replication in the infected cells. Moreover, our data show that ATG5 protein is required to execute DV2-induced autophagy. All together, we are the first to demonstrate that DV can activate autophagic machinery that is favorable for viral replication.

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JO - Virology

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Autophagic machinery activated by dengue virus enhances virus replication

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