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  • 1
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    Immunology and the elusive AIDS vaccine (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-03-12
    Description: Developing a human immunodeficiency virus (HIV) vaccine is critical to end the global acquired immunodeficiency syndrome (AIDS) epidemic, but many question whether this goal is achievable. Natural immunity is not protective, and despite immunogenicity of HIV vaccine candidates, human trials have exclusively yielded disappointing results. Nevertheless, there is an indication that success may be possible, but this will be dependent on understanding the antiviral immune response in unprecedented depth to identify and engineer the types of immunity required. Here we outline fundamental immunological questions that need to be answered to develop a protective HIV vaccine, and the immediate need to harness a much broader scientific community to achieve this goal.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Virgin, Herbert W -- Walker, Bruce D -- England -- Nature. 2010 Mar 11;464(7286):224-31. doi: 10.1038/nature08898.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Washington University School of Medicine and Midwest Regional Center of Excellence for Biodefense and Emerging Infectious Disease Research, Campus Box 8118, 660 South Euclid Avenue, Saint Louis, Missouri 63110, USA. virgin@wustl.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20220841" target="_blank"〉PubMed〈/a〉
    Keywords: *AIDS Vaccines ; Acquired Immunodeficiency Syndrome/*immunology/prevention & control ; Animals ; B-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/immunology ; HIV/*immunology ; HIV Antibodies/immunology ; Humans ; Mucous Membrane/immunology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-12-10
    Description: Mycobacterium tuberculosis, a major global health threat, replicates in macrophages in part by inhibiting phagosome-lysosome fusion, until interferon-gamma (IFNgamma) activates the macrophage to traffic M. tuberculosis to the lysosome. How IFNgamma elicits this effect is unknown, but many studies suggest a role for macroautophagy (herein termed autophagy), a process by which cytoplasmic contents are targeted for lysosomal degradation. The involvement of autophagy has been defined based on studies in cultured cells where M. tuberculosis co-localizes with autophagy factors ATG5, ATG12, ATG16L1, p62, NDP52, BECN1 and LC3 (refs 2-6), stimulation of autophagy increases bacterial killing, and inhibition of autophagy increases bacterial survival. Notably, these studies reveal modest (~1.5-3-fold change) effects on M. tuberculosis replication. By contrast, mice lacking ATG5 in monocyte-derived cells and neutrophils (polymorponuclear cells, PMNs) succumb to M. tuberculosis within 30 days, an extremely severe phenotype similar to mice lacking IFNgamma signalling. Importantly, ATG5 is the only autophagy factor that has been studied during M. tuberculosis infection in vivo and autophagy-independent functions of ATG5 have been described. For this reason, we used a genetic approach to elucidate the role for multiple autophagy-related genes and the requirement for autophagy in resistance to M. tuberculosis infection in vivo. Here we show that, contrary to expectation, autophagic capacity does not correlate with the outcome of M. tuberculosis infection. Instead, ATG5 plays a unique role in protection against M. tuberculosis by preventing PMN-mediated immunopathology. Furthermore, while Atg5 is dispensable in alveolar macrophages during M. tuberculosis infection, loss of Atg5 in PMNs can sensitize mice to M. tuberculosis. These findings shift our understanding of the role of ATG5 during M. tuberculosis infection, reveal new outcomes of ATG5 activity, and shed light on early events in innate immunity that are required to regulate disease pathology and bacterial replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimmey, Jacqueline M -- Huynh, Jeremy P -- Weiss, Leslie A -- Park, Sunmin -- Kambal, Amal -- Debnath, Jayanta -- Virgin, Herbert W -- Stallings, Christina L -- GM007067/GM/NIGMS NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):565-9. doi: 10.1038/nature16451. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/genetics ; Dendritic Cells/immunology/metabolism ; Female ; Immunity, Innate/immunology ; Interferon-gamma/deficiency/immunology ; Macrophages, Alveolar/immunology/metabolism ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/*metabolism ; *Mycobacterium tuberculosis/immunology/physiology ; Neutrophils/*immunology/metabolism ; Tuberculosis/*immunology/microbiology/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis (2012)
    Nature Publishing Group (NPG)
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    Publication Date: 2012-01-20
    Description: Exercise has beneficial effects on human health, including protection against metabolic disorders such as diabetes. However, the cellular mechanisms underlying these effects are incompletely understood. The lysosomal degradation pathway, autophagy, is an intracellular recycling system that functions during basal conditions in organelle and protein quality control. During stress, increased levels of autophagy permit cells to adapt to changing nutritional and energy demands through protein catabolism. Moreover, in animal models, autophagy protects against diseases such as cancer, neurodegenerative disorders, infections, inflammatory diseases, ageing and insulin resistance. Here we show that acute exercise induces autophagy in skeletal and cardiac muscle of fed mice. To investigate the role of exercise-mediated autophagy in vivo, we generated mutant mice that show normal levels of basal autophagy but are deficient in stimulus (exercise- or starvation)-induced autophagy. These mice (termed BCL2 AAA mice) contain knock-in mutations in BCL2 phosphorylation sites (Thr69Ala, Ser70Ala and Ser84Ala) that prevent stimulus-induced disruption of the BCL2-beclin-1 complex and autophagy activation. BCL2 AAA mice show decreased endurance and altered glucose metabolism during acute exercise, as well as impaired chronic exercise-mediated protection against high-fat-diet-induced glucose intolerance. Thus, exercise induces autophagy, BCL2 is a crucial regulator of exercise- (and starvation)-induced autophagy in vivo, and autophagy induction may contribute to the beneficial metabolic effects of exercise.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518436/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3518436/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉He, Congcong -- Bassik, Michael C -- Moresi, Viviana -- Sun, Kai -- Wei, Yongjie -- Zou, Zhongju -- An, Zhenyi -- Loh, Joy -- Fisher, Jill -- Sun, Qihua -- Korsmeyer, Stanley -- Packer, Milton -- May, Herman I -- Hill, Joseph A -- Virgin, Herbert W -- Gilpin, Christopher -- Xiao, Guanghua -- Bassel-Duby, Rhonda -- Scherer, Philipp E -- Levine, Beth -- 1P01 DK0887761/DK/NIDDK NIH HHS/ -- P01 DK088761/DK/NIDDK NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA112023/CA/NCI NIH HHS/ -- R01 DK055758/DK/NIDDK NIH HHS/ -- R0I AI084887/AI/NIAID NIH HHS/ -- R0I HL080244/HL/NHLBI NIH HHS/ -- R0I HL090842/HL/NHLBI NIH HHS/ -- RC1 DK086629/DK/NIDDK NIH HHS/ -- RCI DK086629/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jan 18;481(7382):511-5. doi: 10.1038/nature10758.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Autophagy Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22258505" target="_blank"〉PubMed〈/a〉
    Keywords: Adiponectin/blood ; Animals ; Apoptosis Regulatory Proteins/genetics/metabolism ; Autophagy/drug effects/genetics/*physiology ; Cells, Cultured ; Dietary Fats/adverse effects ; Food Deprivation/physiology ; Gene Knock-In Techniques ; Glucose/*metabolism ; Glucose Intolerance/chemically induced/prevention & control ; Glucose Tolerance Test ; *Homeostasis/drug effects ; Leptin/blood ; Male ; Mice ; Mice, Transgenic ; Muscle, Skeletal/cytology/drug effects/*metabolism ; Mutation ; Myocardium/cytology/*metabolism ; Phosphorylation/genetics ; Physical Conditioning, Animal/*physiology ; Physical Endurance/genetics/physiology ; Physical Exertion/genetics/physiology ; Protein Binding/genetics ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins c-bcl-2 ; Running/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Autophagy in immunity and inflammation (2011)
    Nature Publishing Group (NPG)
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    Publication Date: 2011-01-21
    Description: Autophagy is an essential, homeostatic process by which cells break down their own components. Perhaps the most primordial function of this lysosomal degradation pathway is adaptation to nutrient deprivation. However, in complex multicellular organisms, the core molecular machinery of autophagy - the 'autophagy proteins' - orchestrates diverse aspects of cellular and organismal responses to other dangerous stimuli such as infection. Recent developments reveal a crucial role for the autophagy pathway and proteins in immunity and inflammation. They balance the beneficial and detrimental effects of immunity and inflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131688/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131688/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, Beth -- Mizushima, Noboru -- Virgin, Herbert W -- R01 AI054483/AI/NIAID NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- R01 CA096511/CA/NCI NIH HHS/ -- R01 CA109618/CA/NCI NIH HHS/ -- R01 CA109618-07/CA/NCI NIH HHS/ -- U54 AI057156/AI/NIAID NIH HHS/ -- U54 AI057160/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Jan 20;469(7330):323-35. doi: 10.1038/nature09782.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9113, USA. beth.levine@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248839" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/*immunology/physiology ; Cell Membrane/metabolism ; Humans ; Immunity/*immunology/physiology ; Immunity, Innate/immunology/physiology ; Infection/immunology/microbiology/parasitology/virology ; Inflammation/*immunology/microbiology/*pathology ; Phagosomes/immunology/microbiology/parasitology/virology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Identification of a candidate therapeutic autophagy-inducing peptide (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-01
    Description: The lysosomal degradation pathway of autophagy has a crucial role in defence against infection, neurodegenerative disorders, cancer and ageing. Accordingly, agents that induce autophagy may have broad therapeutic applications. One approach to developing such agents is to exploit autophagy manipulation strategies used by microbial virulence factors. Here we show that a peptide, Tat-beclin 1-derived from a region of the autophagy protein, beclin 1, which binds human immunodeficiency virus (HIV)-1 Nef-is a potent inducer of autophagy, and interacts with a newly identified negative regulator of autophagy, GAPR-1 (also called GLIPR2). Tat-beclin 1 decreases the accumulation of polyglutamine expansion protein aggregates and the replication of several pathogens (including HIV-1) in vitro, and reduces mortality in mice infected with chikungunya or West Nile virus. Thus, through the characterization of a domain of beclin 1 that interacts with HIV-1 Nef, we have developed an autophagy-inducing peptide that has potential efficacy in the treatment of human diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3788641/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3788641/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shoji-Kawata, Sanae -- Sumpter, Rhea -- Leveno, Matthew -- Campbell, Grant R -- Zou, Zhongju -- Kinch, Lisa -- Wilkins, Angela D -- Sun, Qihua -- Pallauf, Kathrin -- MacDuff, Donna -- Huerta, Carlos -- Virgin, Herbert W -- Helms, J Bernd -- Eerland, Ruud -- Tooze, Sharon A -- Xavier, Ramnik -- Lenschow, Deborah J -- Yamamoto, Ai -- King, David -- Lichtarge, Olivier -- Grishin, Nick V -- Spector, Stephen A -- Kaloyanova, Dora V -- Levine, Beth -- K08 AI099150/AI/NIAID NIH HHS/ -- P30 CA142543/CA/NCI NIH HHS/ -- R01 GM066099/GM/NIGMS NIH HHS/ -- R01 GM079656/GM/NIGMS NIH HHS/ -- R01 GM094575/GM/NIGMS NIH HHS/ -- R01 NS050199/NS/NINDS NIH HHS/ -- R01 NS077111/NS/NINDS NIH HHS/ -- R01 NS084912/NS/NINDS NIH HHS/ -- R0I DK083756/DK/NIDDK NIH HHS/ -- R0I DK086502/DK/NIDDK NIH HHS/ -- R0I GM066099/GM/NIGMS NIH HHS/ -- R0I GM079656/GM/NIGMS NIH HHS/ -- R0I NS063973/NS/NINDS NIH HHS/ -- R0I NS077874/NS/NINDS NIH HHS/ -- RC1 DK086502/DK/NIDDK NIH HHS/ -- T32 GM008297/GM/NIGMS NIH HHS/ -- U54 AI057156/AI/NIAID NIH HHS/ -- U54AI057156/AI/NIAID NIH HHS/ -- U54AI057160/AI/NIAID NIH HHS/ -- Cancer Research UK/United Kingdom -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 14;494(7436):201-6. doi: 10.1038/nature11866. Epub 2013 Jan 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Internal Medicine, UT Southwestern Medical Center, Dallas, Texas 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23364696" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Apoptosis Regulatory Proteins/*chemistry/metabolism/pharmacology/*therapeutic use ; Autophagy/*drug effects ; Cell Membrane Permeability ; Cells, Cultured ; Chikungunya virus/drug effects ; HIV-1/drug effects/metabolism/physiology ; HeLa Cells ; Humans ; Macrophages/cytology ; Membrane Proteins/*chemistry/metabolism/pharmacology/*therapeutic use ; Mice ; Molecular Sequence Data ; Peptide Fragments/*chemistry/metabolism/*pharmacology ; Recombinant Fusion Proteins/chemistry/metabolism/pharmacology ; Virus Replication/drug effects ; West Nile virus/drug effects ; nef Gene Products, Human Immunodeficiency Virus/metabolism ; tat Gene Products, Human Immunodeficiency Virus/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Noncanonical autophagy inhibits the autoinflammatory, lupus-like response to dying cells (2016)
    Nature Publishing Group (NPG)
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    Publication Date: 2016-04-21
    Description: Defects in clearance of dying cells have been proposed to underlie the pathogenesis of systemic lupus erythematosus (SLE). Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phagocytes from patients with SLE often display defective clearance and increased inflammatory cytokine production when exposed to dying cells in vitro. Previously, we and others described a form of noncanonical autophagy known as LC3-associated phagocytosis (LAP), in which phagosomes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway to facilitate maturation of phagosomes and digestion of their contents. Genome-wide association studies have identified polymorphisms in the Atg5 (ref. 8) and possibly Atg7 (ref. 9) genes, involved in both canonical autophagy and LAP, as markers of a predisposition for SLE. Here we describe the consequences of defective LAP in vivo. Mice lacking any of several components of the LAP pathway show increased serum levels of inflammatory cytokines and autoantibodies, glomerular immune complex deposition, and evidence of kidney damage. When dying cells are injected into LAP-deficient mice, they are engulfed but not efficiently degraded and trigger acute elevation of pro-inflammatory cytokines but not anti-inflammatory interleukin (IL)-10. Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient, mice accelerated the development of SLE-like disease, including increased serum levels of autoantibodies. By contrast, mice deficient in genes required for canonical autophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production, or SLE-like disease, and, like wild-type mice, produce IL-10 in response to dying cells. Therefore, defects in LAP, rather than canonical autophagy, can cause SLE-like phenomena, and may contribute to the pathogenesis of SLE.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4860026/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martinez, Jennifer -- Cunha, Larissa D -- Park, Sunmin -- Yang, Mao -- Lu, Qun -- Orchard, Robert -- Li, Quan-Zhen -- Yan, Mei -- Janke, Laura -- Guy, Cliff -- Linkermann, Andreas -- Virgin, Herbert W -- Green, Douglas R -- 1ZIAES10328601/PHS HHS/ -- R01 AI040646/AI/NIAID NIH HHS/ -- R01 AI40646/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- ZIA ES103286-01/Intramural NIH HHS/ -- England -- Nature. 2016 May 5;533(7601):115-9. doi: 10.1038/nature17950. Epub 2016 Apr 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA. ; Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, North Carolina 27709, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Division of Nephrology and Hypertension, Christian-Albrechts-University, Kiel 24105, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/27096368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigen-Antibody Complex/metabolism ; Autoantibodies/blood ; *Autophagy/genetics ; Cytokines/biosynthesis/blood ; Inflammation/blood/genetics/*pathology ; Interleukin-10/biosynthesis ; Kidney/metabolism/pathology ; Lupus Erythematosus, Systemic/blood/genetics/*immunology/*pathology ; Male ; Mice ; Microtubule-Associated Proteins/metabolism ; Phagocytes/cytology/physiology ; Phagosomes/physiology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Pan-viral specificity of IFN-induced genes reveals new roles for cGAS in innate immunity (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-29
    Description: The type I interferon (IFN) response protects cells from viral infection by inducing hundreds of interferon-stimulated genes (ISGs), some of which encode direct antiviral effectors. Recent screening studies have begun to catalogue ISGs with antiviral activity against several RNA and DNA viruses. However, antiviral ISG specificity across multiple distinct classes of viruses remains largely unexplored. Here we used an ectopic expression assay to screen a library of more than 350 human ISGs for effects on 14 viruses representing 7 families and 11 genera. We show that 47 genes inhibit one or more viruses, and 25 genes enhance virus infectivity. Comparative analysis reveals that the screened ISGs target positive-sense single-stranded RNA viruses more effectively than negative-sense single-stranded RNA viruses. Gene clustering highlights the cytosolic DNA sensor cyclic GMP-AMP synthase (cGAS, also known as MB21D1) as a gene whose expression also broadly inhibits several RNA viruses. In vitro, lentiviral delivery of enzymatically active cGAS triggers a STING-dependent, IRF3-mediated antiviral program that functions independently of canonical IFN/STAT1 signalling. In vivo, genetic ablation of murine cGAS reveals its requirement in the antiviral response to two DNA viruses, and an unappreciated contribution to the innate control of an RNA virus. These studies uncover new paradigms for the preferential specificity of IFN-mediated antiviral pathways spanning several virus families.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077721/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4077721/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schoggins, John W -- MacDuff, Donna A -- Imanaka, Naoko -- Gainey, Maria D -- Shrestha, Bimmi -- Eitson, Jennifer L -- Mar, Katrina B -- Richardson, R Blake -- Ratushny, Alexander V -- Litvak, Vladimir -- Dabelic, Rea -- Manicassamy, Balaji -- Aitchison, John D -- Aderem, Alan -- Elliott, Richard M -- Garcia-Sastre, Adolfo -- Racaniello, Vincent -- Snijder, Eric J -- Yokoyama, Wayne M -- Diamond, Michael S -- Virgin, Herbert W -- Rice, Charles M -- 099220/Wellcome Trust/United Kingdom -- AI057158/AI/NIAID NIH HHS/ -- AI057160/AI/NIAID NIH HHS/ -- AI083025/AI/NIAID NIH HHS/ -- AI091707/AI/NIAID NIH HHS/ -- AI095611/AI/NIAID NIH HHS/ -- AI104972/AI/NIAID NIH HHS/ -- DK095031/DK/NIDDK NIH HHS/ -- G0801822/Medical Research Council/United Kingdom -- GM076547/GM/NIGMS NIH HHS/ -- GM103511/GM/NIGMS NIH HHS/ -- HHSN266200700010C/PHS HHS/ -- HHSN272200900041CU19/CU/CSP VA/ -- K01 DK095031/DK/NIDDK NIH HHS/ -- R00 AI095320/AI/NIAID NIH HHS/ -- R01 AI032972/AI/NIAID NIH HHS/ -- R01 AI091707/AI/NIAID NIH HHS/ -- R01 AI102597/AI/NIAID NIH HHS/ -- R01 AI104972/AI/NIAID NIH HHS/ -- T32 AI005284/AI/NIAID NIH HHS/ -- T32 AR007279/AR/NIAMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Jan 30;505(7485):691-5. doi: 10.1038/nature12862. Epub 2013 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York 10065, USA [2] Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA (J.W.S.); MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland G61 1QH, UK (R.M.E.). ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York 10065, USA. ; Rheumatology Division, Department of Medicine, and Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Infectious Diseases Division, Department of Medicine and Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; 1] Seattle Biomedical Research Institute, Seattle, Washington 98109, USA [2] Institute for Systems Biology, Seattle, Washington 98109, USA. ; Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. ; Department of Microbiology and Immunology, Columbia University, New York, New York 10032, USA. ; Department of Microbiology, University of Chicago, Chicago, Illinois 60637, USA. ; 1] School of Biology, University of St Andrews, St Andrews, Scotland KY16 9ST, UK [2] Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA (J.W.S.); MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland G61 1QH, UK (R.M.E.). ; 1] Department of Microbiology, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [2] Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA [3] Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA. ; Department of Medical Microbiology, Leiden University Medical Center, Leiden 2300 RC, The Netherlands. ; 1] Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA [2] Infectious Diseases Division, Department of Medicine and Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24284630" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cluster Analysis ; DNA Viruses/immunology/pathogenicity ; Flow Cytometry ; Gene Library ; Immunity, Innate/*genetics/*immunology ; Interferon Regulatory Factor-3/immunology/metabolism ; Interferons/*immunology/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; Nucleotidyltransferases/deficiency/genetics/*immunology/*metabolism ; RNA Viruses/immunology/pathogenicity ; STAT1 Transcription Factor/metabolism ; Substrate Specificity ; Viruses/classification/*immunology/pathogenicity
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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