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      Impact of cellular autophagy on viruses: Insights from hepatitis B virus and human retroviruses

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          Abstract

          Autophagy is a protein degradative process important for normal cellular metabolism. It is apparently used also by cells to eliminate invading pathogens. Interestingly, many pathogens have learned to subvert the cell’s autophagic process. Here, we review the interactions between viruses and cells in regards to cellular autophagy. Using findings from hepatitis B virus and human retroviruses, HIV-1 and HTLV-1, we discuss mechanisms used by viruses to usurp cellular autophagy in ways that benefit viral replication.

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          Tetherin inhibits retrovirus release and is antagonized by HIV-1 Vpu.

          Stuart J D Neil, Trinity Zang, Paul D. Bieniasz (2008)
          Human cells possess an antiviral activity that inhibits the release of retrovirus particles, and other enveloped virus particles, and is antagonized by the HIV-1 accessory protein, Vpu. This antiviral activity can be constitutively expressed or induced by interferon-alpha, and it consists of protein-based tethers, which we term 'tetherins', that cause retention of fully formed virions on infected cell surfaces. Using deductive constraints and gene expression analyses, we identify CD317 (also called BST2 or HM1.24), a membrane protein of previously unknown function, as a tetherin. Specifically, CD317 expression correlated with, and induced, a requirement for Vpu during HIV-1 and murine leukaemia virus particle release. Furthermore, in cells where HIV-1 virion release requires Vpu expression, depletion of CD317 abolished this requirement. CD317 caused retention of virions on cell surfaces and, after endocytosis, in CD317-positive compartments. Vpu co-localized with CD317 and inhibited these effects. Inhibition of Vpu function and consequent mobilization of tetherin's antiviral activity is a potential therapeutic strategy in HIV/AIDS.
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            Autophagy is activated for cell survival after endoplasmic reticulum stress.

            Maiko OGATA, Shin-ichiro Hino, Atsushi Saito … (2006)
            Eukaryotic cells deal with accumulation of unfolded proteins in the endoplasmic reticulum (ER) by the unfolded protein response, involving the induction of molecular chaperones, translational attenuation, and ER-associated degradation, to prevent cell death. Here, we found that the autophagy system is activated as a novel signaling pathway in response to ER stress. Treatment of SK-N-SH neuroblastoma cells with ER stressors markedly induced the formation of autophagosomes, which were recognized at the ultrastructural level. The formation of green fluorescent protein (GFP)-LC3-labeled structures (GFP-LC3 "dots"), representing autophagosomes, was extensively induced in cells exposed to ER stress with conversion from LC3-I to LC3-II. In IRE1-deficient cells or cells treated with c-Jun N-terminal kinase (JNK) inhibitor, the autophagy induced by ER stress was inhibited, indicating that the IRE1-JNK pathway is required for autophagy activation after ER stress. In contrast, PERK-deficient cells and ATF6 knockdown cells showed that autophagy was induced after ER stress in a manner similar to the wild-type cells. Disturbance of autophagy rendered cells vulnerable to ER stress, suggesting that autophagy plays important roles in cell survival after ER stress.
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              Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor.

              Zhenyu Yue, Shengkan Jin, Chingwen Yang … (2003)
              The biochemical properties of beclin 1 suggest a role in two fundamentally important cell biological pathways: autophagy and apoptosis. We show here that beclin 1-/- mutant mice die early in embryogenesis and beclin 1+/- mutant mice suffer from a high incidence of spontaneous tumors. These tumors continue to express wild-type beclin 1 mRNA and protein, establishing that beclin 1 is a haploinsufficient tumor suppressor gene. Beclin 1-/- embryonic stem cells have a severely altered autophagic response, whereas their apoptotic response to serum withdrawal or UV light is normal. These results demonstrate that beclin 1 is a critical component of mammalian autophagy and establish a role for autophagy in tumor suppression. They both provide a biological explanation for recent evidence implicating beclin 1 in human cancer and suggest that mutations in other genes operating in this pathway may contribute to tumor formation through deregulation of autophagy.
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                Author and article information

                Contributors
                Sai-Wen Tang
                Aurelie Ducroux
                Kuan-Teh Jeang
                Christine Neuveut
                Journal
                Journal ID (nlm-ta): J Biomed Sci
                Journal ID (iso-abbrev): J. Biomed. Sci
                Title: Journal of Biomedical Science
                Publisher: BioMed Central
                ISSN (Print): 1021-7770
                ISSN (Electronic): 1423-0127
                Publication date Collection: 2012
                Publication date (Electronic): 30 October 2012
                Volume: 19
                Issue: 1
                Page: 92
                Affiliations
                [1 ]Molecular Virology Section, Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, 20892-0460, USA
                [2 ]Laboratory of Hepacivirus and Innate Immunity, Institut Pasteur, 75015, Paris, France
                Article
                Publisher ID: 1423-0127-19-92
                DOI: 10.1186/1423-0127-19-92
                PMC ID: 3495035
                PubMed ID: 23110561
                SO-VID: 2df8b4ca-08d9-48d6-a6f9-927d71d29c34
                Copyright © Copyright ©2012 Tang et al.; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 2 October 2012
                Date accepted : 12 October 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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