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Special Issue "Autophagy and Viruses"

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (1 June 2011)

Special Issue Editor

Guest Editor
Dr. Sara Cherry (Website)

Department of Microbiology, Penn Genome Frontiers Institute, University of Pennsylvania School of Medicine, 304K Lynch Laboratories, 433 South University Avenue, Philadelphia, PA 19104-6018, USA
Fax: +1 215 746 6697

Published Papers (6 papers)

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Review

Open AccessReview Unconventional Use of LC3 by Coronaviruses through the Alleged Subversion of the ERAD Tuning Pathway
Viruses 2011, 3(9), 1610-1623; doi:10.3390/v3091610
Received: 21 June 2011 / Revised: 15 August 2011 / Accepted: 22 August 2011 / Published: 5 September 2011
Cited by 7 | PDF Full-text (4083 KB)
Abstract
Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by [...] Read more.
Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Open AccessReview Picornavirus Subversion of the Autophagy Pathway
Viruses 2011, 3(9), 1549-1561; doi:10.3390/v3091549
Received: 9 June 2011 / Revised: 9 August 2011 / Accepted: 15 August 2011 / Published: 26 August 2011
Cited by 9 | PDF Full-text (315 KB)
Abstract
While autophagy has been shown to act as an anti-viral defense, the Picornaviridae avoid and, in many cases, subvert this pathway to promote their own replication. Evidence indicates that some picornaviruses hijack autophagy in order to induce autophagosome-like membrane structures for genomic [...] Read more.
While autophagy has been shown to act as an anti-viral defense, the Picornaviridae avoid and, in many cases, subvert this pathway to promote their own replication. Evidence indicates that some picornaviruses hijack autophagy in order to induce autophagosome-like membrane structures for genomic RNA replication. Expression of picornavirus proteins can specifically induce the machinery of autophagy, although the mechanisms by which the viruses employ autophagy appear to differ. Many picornaviruses up-regulate autophagy in order to promote viral replication while some members of the family also inhibit degradation by autolysosomes. Here we explore the unusual relationship of this medically important family of viruses with a degradative mechanism of innate immunity. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Open AccessReview Dengue Virus and Autophagy
Viruses 2011, 3(8), 1332-1341; doi:10.3390/v3081332
Received: 17 June 2011 / Revised: 19 July 2011 / Accepted: 21 July 2011 / Published: 4 August 2011
Cited by 39 | PDF Full-text (652 KB)
Abstract
Several independent groups have published that autophagy is required for optimal RNA replication of dengue virus (DENV). Initially, it was postulated that autophagosomes might play a structural role in replication complex formation. However, cryo-EM tomography of DENV replication complexes showed that DENV replicates [...] Read more.
Several independent groups have published that autophagy is required for optimal RNA replication of dengue virus (DENV). Initially, it was postulated that autophagosomes might play a structural role in replication complex formation. However, cryo-EM tomography of DENV replication complexes showed that DENV replicates on endoplasmic reticulum (ER) cisternae invaginations and not on classical autophagosomes. Recently, it was reported that autophagy plays an indirect role in DENV replication by modulating cellular lipid metabolism. DENV-induced autophagosomes deplete cellular triglycerides that are stored in lipid droplets, leading to increased β-oxidation and energy production. This is the first example of a virus triggering autophagy to modulate cellular physiology. In this review, we summarize these data and discuss new questions and implications for autophagy during DENV replication. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Open AccessReview Impact of the Autophagy Machinery on Hepatitis C Virus Infection
Viruses 2011, 3(8), 1342-1357; doi:10.3390/v3081342
Received: 16 June 2011 / Revised: 20 July 2011 / Accepted: 21 July 2011 / Published: 4 August 2011
Cited by 24 | PDF Full-text (147 KB)
Abstract
Autophagy is a cellular process that catabolizes cytoplasmic components and maintains energy homeostasis. As a stress response, the autophagy machinery interconnects a wide range of cellular pathways, enhancing the spread of certain pathogens while limiting others, and has become a highly active [...] Read more.
Autophagy is a cellular process that catabolizes cytoplasmic components and maintains energy homeostasis. As a stress response, the autophagy machinery interconnects a wide range of cellular pathways, enhancing the spread of certain pathogens while limiting others, and has become a highly active research area over the past several years. Independent laboratories have recently reported that autophagy vesicles accumulate in hepatitis C virus (HCV) infected cells and that autophagy proteins can function as proviral factors required for HCV replication. In this review, we summarize what is currently known about the interplay between autophagy and HCV and the possible mechanisms whereby autophagy proteins might favor HCV propagation. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Figures

Open AccessReview Viruses, Autophagy Genes, and Crohn’s Disease
Viruses 2011, 3(7), 1281-1311; doi:10.3390/v3071281
Received: 8 June 2011 / Revised: 12 July 2011 / Accepted: 13 July 2011 / Published: 21 July 2011
Cited by 12 | PDF Full-text (955 KB)
Abstract
The etiology of the intestinal disease Crohn’s disease involves genetic factors as well as ill-defined environmental agents. Several genetic variants linked to this disease are associated with autophagy, a process that is critical for proper responses to viral infections. While a role [...] Read more.
The etiology of the intestinal disease Crohn’s disease involves genetic factors as well as ill-defined environmental agents. Several genetic variants linked to this disease are associated with autophagy, a process that is critical for proper responses to viral infections. While a role for viruses in this disease remains speculative, accumulating evidence indicate that this possibility requires serious consideration. In this review, we will examine the three-way relationship between viruses, autophagy genes, and Crohn’s disease and discuss how host-pathogen interactions can mediate complex inflammatory disorders. Full article
(This article belongs to the Special Issue Autophagy and Viruses)
Open AccessReview Beclin-1 Targeting for Viral Immune Escape
Viruses 2011, 3(7), 1166-1178; doi:10.3390/v3071166
Received: 23 June 2011 / Revised: 4 July 2011 / Accepted: 5 July 2011 / Published: 12 July 2011
Cited by 19 | PDF Full-text (302 KB)
Abstract
Macroautophagy is a catabolic pathway in eukaryotic cells that has recently been shown to facilitate pathogen detection, pathogen restriction and pathogen-derived antigen presentation to CD4+ T cells. Due to these protective functions during immune responses, several pathogens, including RNA and DNA [...] Read more.
Macroautophagy is a catabolic pathway in eukaryotic cells that has recently been shown to facilitate pathogen detection, pathogen restriction and pathogen-derived antigen presentation to CD4+ T cells. Due to these protective functions during immune responses, several pathogens, including RNA and DNA viruses, have developed strategies to inhibit autophagosome generation or maturation. Interestingly, most of the respective viral proteins exert these functions via binding to Beclin-1, an essential macroautophagy protein that constitutes part of the phosphatidylinositol-3 kinase complexes that mark membranes for autophagosome generation and facilitate autophagosome fusion with lyososomes. The viruses that inhibit macroautophagy by this pathway include herpesviruses, HIV and influenza A virus. Inhibition either before or after autophagosome formation seems to benefit their viral replication by different mechanisms, which are discussed here. Full article
(This article belongs to the Special Issue Autophagy and Viruses)

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