Autophagy Protects against Sindbis Virus Infection of the Central Nervous System
Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be causally established. Here, we report that the autophagy gene Atg5 function is critical for protection against lethal Sindbis virus (SIN) infect...
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| Published in | Cell host & microbe Vol. 7; no. 2; pp. 115 - 127 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
18.02.2010
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1931-3128 1934-6069 1934-6069 |
| DOI | 10.1016/j.chom.2010.01.007 |
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| Abstract | Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be causally established. Here, we report that the autophagy gene Atg5 function is critical for protection against lethal Sindbis virus (SIN) infection of the mouse central nervous system. Inactivating Atg5 in SIN-infected neurons results in delayed clearance of viral proteins, increased accumulation of the cellular p62 adaptor protein, and increased cell death in neurons, but the levels of viral replication remain unaltered. In vitro, p62 interacts with SIN capsid protein, and genetic knockdown of p62 blocks the targeting of viral capsid to autophagosomes. Moreover, p62 or autophagy gene knockdown increases viral capsid accumulation and accelerates virus-induced cell death without affecting virus replication. These results suggest a function for autophagy in mammalian antiviral defense: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival. |
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| AbstractList | Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be causally established. Here, we report that the autophagy gene Atg5 function is critical for protection against lethal Sindbis virus (SIN) infection of the mouse central nervous system. Inactivating Atg5 in SIN-infected neurons results in delayed clearance of viral proteins, increased accumulation of the cellular p62 adaptor protein, and increased cell death in neurons, but the levels of viral replication remain unaltered. In vitro, p62 interacts with SIN capsid protein, and genetic knockdown of p62 blocks the targeting of viral capsid to autophagosomes. Moreover, p62 or autophagy gene knockdown increases viral capsid accumulation and accelerates virus-induced cell death without affecting virus replication. These results suggest a function for autophagy in mammalian antiviral defense: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival.Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be causally established. Here, we report that the autophagy gene Atg5 function is critical for protection against lethal Sindbis virus (SIN) infection of the mouse central nervous system. Inactivating Atg5 in SIN-infected neurons results in delayed clearance of viral proteins, increased accumulation of the cellular p62 adaptor protein, and increased cell death in neurons, but the levels of viral replication remain unaltered. In vitro, p62 interacts with SIN capsid protein, and genetic knockdown of p62 blocks the targeting of viral capsid to autophagosomes. Moreover, p62 or autophagy gene knockdown increases viral capsid accumulation and accelerates virus-induced cell death without affecting virus replication. These results suggest a function for autophagy in mammalian antiviral defense: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival. Autophagy functions in antiviral immunity. However, it is not yet known whether endogenous autophagy genes protect against viral disease in vertebrates. Using three different approaches to inactivate the autophagy gene Atg5 in virally-infected neurons, we found that loss of Atg5 function increases mouse susceptibility to lethal Sindbis virus CNS infection. This phenotype is associated with delayed clearance of viral proteins, increased accumulation of the cellular p62 adaptor protein, and increased cell death in neurons, but not with altered levels of CNS viral replication. In vitro , p62 interacts with Sindbis virus capsid protein and genetic knockdown of p62 blocks the targeting of viral capsid to autophagosomes. Moreover, p62 or autophagy gene knockdown increases viral capsid accumulation and accelerates virus-induced cell death without affecting virus replication. These results suggest a novel function for autophagy in mammalian antiviral defense: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival. Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be causally established. Here, we report that the autophagy gene Atg5 function is critical for protection against lethal Sindbis virus (SIN) infection of the mouse central nervous system. Inactivating Atg5 in SIN-infected neurons results in delayed clearance of viral proteins, increased accumulation of the cellular p62 adaptor protein, and increased cell death in neurons, but the levels of viral replication remain unaltered. In vitro, p62 interacts with SIN capsid protein, and genetic knockdown of p62 blocks the targeting of viral capsid to autophagosomes. Moreover, p62 or autophagy gene knockdown increases viral capsid accumulation and accelerates virus-induced cell death without affecting virus replication. These results suggest a function for autophagy in mammalian antiviral defense: a cell-autonomous mechanism in which p62 adaptor-mediated autophagic viral protein clearance promotes cell survival. |
| Author | Tallóczy, Zsolt Sumpter, Rhea Orvedahl, Anthony Zou, Zhongju MacPherson, Sarah Levine, Beth |
| AuthorAffiliation | 2 Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 1 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 4 Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032 3 Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 |
| AuthorAffiliation_xml | – name: 1 Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 – name: 3 Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 – name: 4 Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032 – name: 2 Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA, 75390 |
| Author_xml | – sequence: 1 givenname: Anthony surname: Orvedahl fullname: Orvedahl, Anthony – sequence: 2 givenname: Sarah surname: MacPherson fullname: MacPherson, Sarah – sequence: 3 givenname: Rhea surname: Sumpter fullname: Sumpter, Rhea – sequence: 4 givenname: Zsolt surname: Tallóczy fullname: Tallóczy, Zsolt – sequence: 5 givenname: Zhongju surname: Zou fullname: Zou, Zhongju – sequence: 6 givenname: Beth surname: Levine fullname: Levine, Beth |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20159618$$D View this record in MEDLINE/PubMed |
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| Snippet | Autophagy functions in antiviral immunity. However, the ability of endogenous autophagy genes to protect against viral disease in vertebrates remains to be... Autophagy functions in antiviral immunity. However, it is not yet known whether endogenous autophagy genes protect against viral disease in vertebrates. Using... |
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| SubjectTerms | Alphavirus Infections - immunology Animals Apoptosis Autophagy Autophagy-Related Protein 5 Cell Line Central Nervous System - physiology Mice Mice, Knockout Microtubule-Associated Proteins - deficiency Microtubule-Associated Proteins - physiology Neurons - pathology Neurons - virology Sindbis Virus - immunology Survival Analysis |
| Title | Autophagy Protects against Sindbis Virus Infection of the Central Nervous System |
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