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      Autophagic machinery activated by dengue virus enhances virus replication

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          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.

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          Dissection of Autophagosome Formation Using Apg5-Deficient Mouse Embryonic Stem Cells

          Noboru Mizushima, Akitsugu Yamamoto, Masahiko Hatano … (2001)
          In macroautophagy, cytoplasmic components are delivered to lysosomes for degradation via autophagosomes that are formed by closure of cup-shaped isolation membranes. However, how the isolation membranes are formed is poorly understood. We recently found in yeast that a novel ubiquitin-like system, the Apg12-Apg5 conjugation system, is essential for autophagy. Here we show that mouse Apg12-Apg5 conjugate localizes to the isolation membranes in mouse embryonic stem cells. Using green fluorescent protein–tagged Apg5, we revealed that the cup-shaped isolation membrane is developed from a small crescent-shaped compartment. Apg5 localizes on the isolation membrane throughout its elongation process. To examine the role of Apg5, we generated Apg5-deficient embryonic stem cells, which showed defects in autophagosome formation. The covalent modification of Apg5 with Apg12 is not required for its membrane targeting, but is essential for involvement of Apg5 in elongation of the isolation membranes. We also show that Apg12-Apg5 is required for targeting of a mammalian Aut7/Apg8 homologue, LC3, to the isolation membranes. These results suggest that the Apg12-Apg5 conjugate plays essential roles in isolation membrane development.
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            Endogenous MHC class II processing of a viral nuclear antigen after autophagy.

            Casper Paludan, Dorothee Schmid, Markus Landthaler … (2005)
            CD4+ T cells classically recognize antigens that are endocytosed and processed in lysosomes for presentation on major histocompatibility complex (MHC) class II molecules. Here, endogenous Epstein-Barr virus nuclear antigen 1 (EBNA1) was found to gain access to this pathway by autophagy. On inhibition of lysosomal acidification, EBNA1, the dominant CD4+ T cell antigen of latent Epstein-Barr virus infection, slowly accumulated in cytosolic autophagosomes. In addition, inhibition of autophagy decreased recognition by EBNA1-specific CD4+ T cell clones. Thus, lysosomal processing after autophagy may contribute to MHC class II-restricted surveillance of long-lived endogenous antigens including nuclear proteins relevant to disease.
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              The Atg5 Atg12 conjugate associates with innate antiviral immune responses.

              Nao Jounai, Fumihiko Takeshita, Kouji Kobiyama … (2007)
              Autophagy is an essential process for physiological homeostasis, but its role in viral infection is only beginning to be elucidated. We show here that the Atg5-Atg12 conjugate, a key regulator of the autophagic process, plays an important role in innate antiviral immune responses. Atg5-deficient mouse embryonic fibroblasts (MEFs) were resistant to vesicular stomatitis virus replication, which was largely due to hyperproduction of type I interferons in response to immunostimulatory RNA (isRNA), such as virus-derived, double-stranded, or 5'-phosphorylated RNA. Similar hyperresponse to isRNA was also observed in Atg7-deficient MEFs, in which Atg5-Atg12 conjugation is impaired. Overexpression of Atg5 or Atg12 resulted in Atg5-Atg12 conjugate formation and suppression of isRNA-mediated signaling. Molecular interaction studies indicated that the Atg5-Atg12 conjugate negatively regulates the type I IFN production pathway by direct association with the retinoic acid-inducible gene I (RIG-I) and IFN-beta promoter stimulator 1 (IPS-1) through the caspase recruitment domains (CARDs). Thus, in contrast to its role in promoting the bactericidal process, a component of the autophagic machinery appears to block innate antiviral immune responses, thereby contributing to RNA virus replication in host cells.
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                Author and article information

                Contributors
                Hsiao-Sheng Liu
                Journal
                Journal ID (nlm-ta): Virology
                Journal ID (iso-abbrev): Virology
                Title: Virology
                Publisher: Academic Press
                ISSN (Print): 0042-6822
                ISSN (Electronic): 1096-0341
                Publication date PMC-release: 18 March 2008
                Publication date (Print): 10 May 2008
                Publication date (Electronic): 18 March 2008
                Volume: 374
                Issue: 2
                Pages: 240-248
                Affiliations
                [a ]Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                [b ]Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                [c ]Tainan Hospital, Department of Health, Executive Yuan, Tainan, Taiwan
                [d ]Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                [e ]Department of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                [f ]Department of Pediatrics, College of Medicine, National Cheng Kung University, Tainan, Taiwan
                Author notes
                [* ]Corresponding author. Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, 1 University Road, Tainan, Taiwan 70101. Fax: +886 6 208 2705. a713@ 123456mail.ncku.edu.tw
                Article
                Publisher ID: S0042-6822(08)00112-8
                DOI: 10.1016/j.virol.2008.02.016
                PMC ID: 7103294
                PubMed ID: 18353420
                SO-VID: b98efc11-4751-4f22-b0e2-6f1056dd7fd9
                Copyright © Copyright © 2008 Elsevier Inc. All rights reserved.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 21 November 2007
                Date revision received : 23 December 2007
                Date accepted : 8 February 2008
                Categories
                Subject: Article

                ScienceOpen disciplines: Microbiology & Virology
                Keywords: dengue virus,autophagy,autophagosome,viral replication
                Data availability:
                ScienceOpen disciplines: Microbiology & Virology
                Keywords: dengue virus, autophagy, autophagosome, viral replication

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