Autoantibodies against type I IFNs in patients with life-threatening COVID-19
The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induc...
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| Published in | Science (American Association for the Advancement of Science) Vol. 370; no. 6515; p. 423 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
The American Association for the Advancement of Science
23.10.2020
American Association for the Advancement of Science (AAAS) American Association for the Advancement of Science |
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| Online Access | Get full text |
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| Abstract | The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang
et al.
used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard
et al.
identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified.
Science
, this issue p.
eabd4570
, p.
eabd4585
; see also p.
404
In a large immunological and genomics study of COVID-19 patients, autoantibodies to type 1 interferons correlated with outcomes.
Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. |
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| AbstractList | The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang
et al.
used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard
et al.
identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified.
Science
, this issue p.
eabd4570
, p. eabd4585; see also p.
404
In a large immunological and genomics study of COVID-19 patients, autoantibodies to type 1 interferons correlated with outcomes.
Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang et al. used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard et al. identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified. Science , this issue p. eabd4570 , p. eabd4585 ; see also p. 404 In a large immunological and genomics study of COVID-19 patients, autoantibodies to type 1 interferons correlated with outcomes. Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men.Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. The genetics underlying severe COVID-19The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs can be more susceptible to infectious diseases. Furthermore, the autoantibody system dampens IFN response to prevent damage from pathogen-induced inflammation. Two studies now examine the likelihood that genetics affects the risk of severe coronavirus disease 2019 (COVID-19) through components of this system (see the Perspective by Beck and Aksentijevich). Q. Zhang et al. used a candidate gene approach and identified patients with severe COVID-19 who have mutations in genes involved in the regulation of type I and III IFN immunity. They found enrichment of these genes in patients and conclude that genetics may determine the clinical course of the infection. Bastard et al. identified individuals with high titers of neutralizing autoantibodies against type I IFN-α2 and IFN-ω in about 10% of patients with severe COVID-19 pneumonia. These autoantibodies were not found either in infected people who were asymptomatic or had milder phenotype or in healthy individuals. Together, these studies identify a means by which individuals at highest risk of life-threatening COVID-19 can be identified.Science, this issue p. eabd4570, p. eabd4585; see also p. 404INTRODUCTIONInterindividual clinical variability is vast in humans infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), ranging from silent infection to rapid death. Three risk factors for life-threatening coronavirus disease 2019 (COVID-19) pneumonia have been identified—being male, being elderly, or having other medical conditions—but these risk factors cannot explain why critical disease remains relatively rare in any given epidemiological group. Given the rising toll of the COVID-19 pandemic in terms of morbidity and mortality, understanding the causes and mechanisms of life-threatening COVID-19 is crucial.RATIONALEB cell autoimmune infectious phenocopies of three inborn errors of cytokine immunity exist, in which neutralizing autoantibodies (auto-Abs) against interferon-γ (IFN-γ) (mycobacterial disease), interleukin-6 (IL-6) (staphylococcal disease), and IL-17A and IL-17F (mucocutaneous candidiasis) mimic the clinical phenotypes of germline mutations of the genes that encode the corresponding cytokines or receptors. Human inborn errors of type I IFNs underlie severe viral respiratory diseases. Neutralizing auto-Abs against type I IFNs, which have been found in patients with a few underlying noninfectious conditions, have not been unequivocally shown to underlie severe viral infections. While searching for inborn errors of type I IFN immunity in patients with life-threatening COVID-19 pneumonia, we also tested the hypothesis that neutralizing auto-Abs against type I IFNs may underlie critical COVID-19. We searched for auto-Abs against type I IFNs in 987 patients hospitalized for life-threatening COVID-19 pneumonia, 663 asymptomatic or mildly affected individuals infected with SARS-CoV-2, and 1227 healthy controls from whom samples were collected before the COVID-19 pandemic.RESULTSAt least 101 of 987 patients (10.2%) with life-threatening COVID-19 pneumonia had neutralizing immunoglobulin G (IgG) auto-Abs against IFN-ω (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three individual type I IFNs. These auto-Abs neutralize high concentrations of the corresponding type I IFNs, including their ability to block SARS-CoV-2 infection in vitro. Moreover, all of the patients tested had low or undetectable serum IFN-α levels during acute disease. These auto-Abs were present before infection in the patients tested and were absent from 663 individuals with asymptomatic or mild SARS-CoV-2 infection (P < 10−16). They were present in only 4 of 1227 (0.33%) healthy individuals (P < 10−16) before the pandemic. The patients with auto-Abs were 25 to 87 years old (half were over 65) and of various ancestries. Notably, 95 of the 101 patients with auto-Abs were men (94%).CONCLUSIONA B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. In these patients, adaptive autoimmunity impairs innate and intrinsic antiviral immunity. These findings provide a first explanation for the excess of men among patients with life-threatening COVID-19 and the increase in risk with age. They also provide a means of identifying individuals at risk of developing life-threatening COVID-19 and ensuring their enrolment in vaccine trials. Finally, they pave the way for prevention and treatment, including plasmapheresis, plasmablast depletion, and recombinant type I IFNs not targeted by the auto-Abs (e.g., IFN-β).Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least 101 of 987 patients with life-threatening coronavirus disease 2019 (COVID-19) pneumonia had neutralizing immunoglobulin G (IgG) autoantibodies (auto-Abs) against interferon-ω (IFN-ω) (13 patients), against the 13 types of IFN-α (36), or against both (52) at the onset of critical disease; a few also had auto-Abs against the other three type I IFNs. The auto-Abs neutralize the ability of the corresponding type I IFNs to block SARS-CoV-2 infection in vitro. These auto-Abs were not found in 663 individuals with asymptomatic or mild SARS-CoV-2 infection and were present in only 4 of 1227 healthy individuals. Patients with auto-Abs were aged 25 to 87 years and 95 of the 101 were men. A B cell autoimmune phenocopy of inborn errors of type I IFN immunity accounts for life-threatening COVID-19 pneumonia in at least 2.6% of women and 12.5% of men. |
| Author | Dorgham, Karim Martinez-Picado, Javier Lampasona, Vito Belot, Alexandre Holland, Steven M. Rice, Charles M. Kerner, Gaspard Lorenzo, Lazaro Cohen, Jeffrey I. Oler, Andrew J. Philippot, Quentin Gu, Jingwen Bettini, Laura Rachele Lionakis, Michail S. Ursini, Matilde Valeria Duval, Xavier Zhang, Qian Shaw, Elana Quintana-Murci, Lluis Vinh, Donald C. Spaan, András N. Aiuti, Alessandro Boisson-Dupuis, Stéphanie Abers, Michael S. Terrier, Benjamin Dalmau, David Cobat, Aurélie Zhang, Yu Ciceri, Fabio Delmonte, Ottavia M. Peterson, Pärt van de Beek, Diederik Brodin, Petter Sottini, Alessandra Imberti, Luisa Rosain, Jérémie Bolze, Alexandre Paghera, Simone Kallaste, Anne D'Angio, Mariella Bigio, Benedetta Montagna, Daniela Vasse, Marc Tsang, John S. Rossi, Camillo Goldbach-Mansky, Raphaela Yang, Rui Michailidis, Eleftherios Bizien, Lucy Le Pen, Jeremie Haerynck, Filomeen Hoffmann, Hans-Heinrich Tangye, Stuart G. Su, Helen C. Husebye, Eystein S. de Jesus, Adriana Almeida Duffy, Darragh Rosen, Lindsey B. Piemonti, Lorenzo Béziat, Vivien Arias, Andrés Augu |
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organization: Helix, San Mateo, CA, USA – sequence: 30 givenname: András N. orcidid: 0000-0001-5981-7259 surname: Spaan fullname: Spaan, András N. organization: St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA., Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, Netherlands – sequence: 31 givenname: Ottavia M. surname: Delmonte fullname: Delmonte, Ottavia M. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 32 givenname: Michael S. surname: Abers fullname: Abers, Michael S. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 33 givenname: Alessandro orcidid: 0000-0002-5398-1717 surname: Aiuti fullname: Aiuti, Alessandro organization: IRCCS San Raffaele Hospital and Vita-Salute San Raffaele University, Milan, Italy – sequence: 34 givenname: Giorgio surname: Casari fullname: Casari, Giorgio organization: IRCCS San Raffaele Hospital and Vita-Salute San Raffaele University, Milan, Italy – sequence: 35 givenname: Vito orcidid: 0000-0001-5162-8445 surname: Lampasona fullname: Lampasona, Vito organization: IRCCS San Raffaele Hospital and Vita-Salute San Raffaele University, Milan, Italy – sequence: 36 givenname: Lorenzo orcidid: 0000-0002-2172-2198 surname: Piemonti fullname: Piemonti, Lorenzo organization: IRCCS San Raffaele Hospital and Vita-Salute San Raffaele University, Milan, Italy – sequence: 37 givenname: Fabio surname: Ciceri fullname: Ciceri, Fabio organization: IRCCS San Raffaele Hospital and Vita-Salute San Raffaele University, Milan, Italy – sequence: 38 givenname: Kaya orcidid: 0000-0002-7313-7652 surname: Bilguvar fullname: Bilguvar, Kaya organization: Department of Genetics, Yale University School of Medicine, New Haven, CT, USA – sequence: 39 givenname: Richard P. surname: Lifton fullname: Lifton, Richard P. organization: Department of Genetics, Yale University School of Medicine, New Haven, CT, USA., Yale Center for Genome Analysis, Yale University School of Medicine, New Haven, CT, USA., Laboratory of Human Genetics and Genomics, The Rockefeller University, New York, NY, USA – sequence: 40 givenname: Marc surname: Vasse fullname: Vasse, Marc organization: Service de Biologie Clinique and UMR-S 1176, Hôpital Foch, Suresnes, France – sequence: 41 givenname: David M. surname: Smadja fullname: Smadja, David M. organization: INSERM UMR-S 1140, Biosurgical Research Laboratory (Carpentier Foundation), Paris University and European Georges Pompidou Hospital, Paris, France – sequence: 42 givenname: Mélanie orcidid: 0000-0003-3062-1214 surname: Migaud fullname: Migaud, Mélanie organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France – sequence: 43 givenname: Jérome orcidid: 0000-0002-2520-3272 surname: Hadjadj fullname: Hadjadj, Jérome organization: Laboratory of Immunogenetics of Pediatric Autoimmune Diseases, INSERM UMR 1163, University of Paris, Imagine Institute, Paris, France – sequence: 44 givenname: Benjamin orcidid: 0000-0001-6612-7336 surname: Terrier fullname: Terrier, Benjamin organization: Department of Internal Medicine, National Referral Center for Rare Systemic Autoimmune Diseases, Assistance Publique Hôpitaux de Paris-Centre (APHP-CUP), University of Paris, Paris, France – sequence: 45 givenname: Darragh orcidid: 0000-0002-8875-2308 surname: Duffy fullname: Duffy, Darragh organization: Translational Immunology Laboratory, Institut Pasteur, Paris, France – sequence: 46 givenname: Lluis orcidid: 0000-0003-2429-6320 surname: Quintana-Murci fullname: Quintana-Murci, Lluis organization: Human Evolutionary Genetics Unit, Institut Pasteur, CNRS UMR 2000, 75015, Paris, France., Human Genomics and Evolution, Collège de France, Paris, France – sequence: 47 givenname: Diederik orcidid: 0000-0002-4571-044X surname: van de Beek fullname: van de Beek, Diederik organization: Amsterdam UMC, University of Amsterdam, Department of Neurology, Amsterdam Neuroscience, Amsterdam, Netherlands – sequence: 48 givenname: Lucie orcidid: 0000-0001-5355-702X surname: Roussel fullname: Roussel, Lucie organization: Department of Medicine, Division of Infectious Diseases, McGill University Health Centre, Montréal, Québec, Canada., Infectious Disease Susceptibility Program, Research Institute, McGill University Health Centre, Montréal, Québec, Canada – sequence: 49 givenname: Donald C. orcidid: 0000-0003-1347-7767 surname: Vinh fullname: Vinh, Donald C. organization: Department of Medicine, Division of Infectious Diseases, McGill University Health Centre, Montréal, Québec, Canada., Infectious Disease Susceptibility Program, Research Institute, McGill University Health Centre, Montréal, Québec, Canada – sequence: 50 givenname: Stuart G. orcidid: 0000-0002-5360-5180 surname: Tangye fullname: Tangye, Stuart G. organization: Garvan Institute of Medical Research, Darlinghurst 2010, NSW, Sydney, Australia., St Vincent’s Clinical School, Faculty of Medicine, University of New South Wales Sydney, Darlinghurst 2010, NSW, Australia – sequence: 51 givenname: Filomeen surname: Haerynck fullname: Haerynck, Filomeen organization: Department of Paediatric Immunology and Pulmonology, Centre for Primary Immunodeficiency Ghent (CPIG), PID Research Laboratory, Jeffrey Modell Diagnosis and Research Centre, Ghent University Hospital, Ghent, Belgium – sequence: 52 givenname: David orcidid: 0000-0003-1936-478X surname: Dalmau fullname: Dalmau, David organization: Infectious Diseases and HIV Service, Hospital Universitari Mutua Terrassa, Universitat de Barcelona, Fundació Docència i Recerca Mutua Terrassa, Terrassa, Barcelona, Catalonia, Spain – sequence: 53 givenname: Javier orcidid: 0000-0002-4916-2129 surname: Martinez-Picado fullname: Martinez-Picado, Javier organization: IrsiCaixa AIDS Research Institute and Institute for Health Science Research Germans Trias i Pujol (IGTP), Badalona, Spain., Infectious Diseases and Immunity, Centre for Health and Social Care Research (CESS), Faculty of Medicine, University of Vic-Central University of Catalonia (UVic-UCC), Vic, Spain., Catalan Institution for Research and Advanced Studies (ICREA), Barcelona, Spain – sequence: 54 givenname: Petter orcidid: 0000-0002-8103-0046 surname: Brodin fullname: Brodin, Petter organization: Science for Life Laboratory, Department of Women's and Children's Health, Karolinska Institutet, Karolinska, Sweden., Department of Pediatric Rheumatology, Karolinska University Hospital, Karolinska, Sweden – sequence: 55 givenname: Michel C. orcidid: 0000-0003-0592-8564 surname: Nussenzweig fullname: Nussenzweig, Michel C. organization: Laboratory of Molecular Immunology, The Rockefeller University, New York, NY, USA., Howard Hughes Medical Institute, New York, NY, USA – sequence: 56 givenname: Stéphanie orcidid: 0000-0002-7115-116X surname: Boisson-Dupuis fullname: Boisson-Dupuis, Stéphanie organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 57 givenname: Carlos orcidid: 0000-0002-4344-8644 surname: Rodríguez-Gallego fullname: Rodríguez-Gallego, Carlos organization: Department of Immunology, Hospital Universitario de Gran Canaria Dr. Negrín, Canarian Health System, Las Palmas de Gran Canaria, Spain., Department of Clinical Sciences, University Fernando Pessoa Canarias, Las Palmas de Gran Canaria, Spain – sequence: 58 givenname: Guillaume surname: Vogt fullname: Vogt, Guillaume organization: Neglected Human Genetics Laboratory, INSERM, University of Paris, Paris, France – sequence: 59 givenname: Trine H. orcidid: 0000-0002-1853-9704 surname: Mogensen fullname: Mogensen, Trine H. organization: Department of Infectious Diseases, Aarhus University Hospital, Skejby, Denmark., Department of Biomedicine, Aarhus University, Aarhus, Denmark – sequence: 60 givenname: Andrew J. orcidid: 0000-0002-6310-0434 surname: Oler fullname: Oler, Andrew J. organization: Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, NIAID, NIH, Bethesda, MD, USA – sequence: 61 givenname: Jingwen surname: Gu fullname: Gu, Jingwen organization: Bioinformatics and Computational Biosciences Branch, Office of Cyber Infrastructure and Computational Biology, NIAID, NIH, Bethesda, MD, USA – sequence: 62 givenname: Peter D. orcidid: 0000-0003-1717-048X surname: Burbelo fullname: Burbelo, Peter D. organization: Division of Intramural Research, National Institute of Dental Craniofacial Research (NIDCR), NIH, Bethesda, MD, USA – sequence: 63 givenname: Jeffrey I. orcidid: 0000-0003-0238-7176 surname: Cohen fullname: Cohen, Jeffrey I. organization: Laboratory of Infectious Diseases, Division of Intramural Research, NIAID, NIH, Bethesda, MD, USA – sequence: 64 givenname: Andrea surname: Biondi fullname: Biondi, Andrea organization: Pediatric Department and Centro Tettamanti-European Reference Network PaedCan, EuroBloodNet, MetabERN-University of Milano-Bicocca-Fondazione MBBM-Ospedale, San Gerardo, Monza, Italy – sequence: 65 givenname: Laura Rachele orcidid: 0000-0002-0280-1704 surname: Bettini fullname: Bettini, Laura Rachele organization: Pediatric Department and Centro Tettamanti-European Reference Network PaedCan, EuroBloodNet, MetabERN-University of Milano-Bicocca-Fondazione MBBM-Ospedale, San Gerardo, Monza, Italy – sequence: 66 givenname: Mariella surname: D'Angio fullname: D'Angio, Mariella organization: Pediatric Department and Centro Tettamanti-European Reference Network PaedCan, EuroBloodNet, MetabERN-University of Milano-Bicocca-Fondazione MBBM-Ospedale, San Gerardo, Monza, Italy – sequence: 67 givenname: Paolo orcidid: 0000-0001-7289-8823 surname: Bonfanti fullname: Bonfanti, Paolo organization: Department of Infectious Diseases, San Gerardo Hospital - University of Milano-Bicocca, Monza, Italy – sequence: 68 givenname: Patrick surname: Rossignol fullname: Rossignol, Patrick organization: University of Lorraine, Plurithematic Clinical Investigation Centre INSERM CIC-P 1433, INSERM U1116, CHRU Nancy Hopitaux de Brabois, F-CRIN INI-CRCT (Cardiovascular and Renal Clinical Trialists), Nancy, France – sequence: 69 givenname: Julien surname: Mayaux fullname: Mayaux, Julien organization: Intensive Care Unit, Pitié-Salpétrière Hospital, Paris University, AP-HP, Paris, France – sequence: 70 givenname: Frédéric orcidid: 0000-0001-7858-7866 surname: Rieux-Laucat fullname: Rieux-Laucat, Frédéric organization: Laboratory of Immunogenetics of Pediatric Autoimmune Diseases, INSERM UMR 1163, University of Paris, Imagine Institute, Paris, France – sequence: 71 givenname: Eystein S. orcidid: 0000-0002-7886-2976 surname: Husebye fullname: Husebye, Eystein S. organization: Department of Clinical Science and K.G. Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway., Department of Medicine, Haukeland University Hospital, Bergen, Norway., Department of Medicine (Solna), Karolinska Institutet, Stockholm, Sweden – sequence: 72 givenname: Francesca surname: Fusco fullname: Fusco, Francesca organization: Human Molecular Genetics Laboratory, Institute of Genetics and Biophysics, “A. Buzzati-Traverso” Consiglio Nazionale delle Ricerche, Naples, Italy – sequence: 73 givenname: Matilde Valeria surname: Ursini fullname: Ursini, Matilde Valeria organization: Human Molecular Genetics Laboratory, Institute of Genetics and Biophysics, “A. Buzzati-Traverso” Consiglio Nazionale delle Ricerche, Naples, Italy – sequence: 74 givenname: Luisa surname: Imberti fullname: Imberti, Luisa organization: Centro di Ricerca Emato-oncologica AIL (CREA) Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy – sequence: 75 givenname: Alessandra surname: Sottini fullname: Sottini, Alessandra organization: Centro di Ricerca Emato-oncologica AIL (CREA) Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy – sequence: 76 givenname: Simone surname: Paghera fullname: Paghera, Simone organization: Centro di Ricerca Emato-oncologica AIL (CREA) Laboratory, Diagnostic Department, ASST Spedali Civili di Brescia, Brescia, Italy – sequence: 77 givenname: Eugenia surname: Quiros-Roldan fullname: Quiros-Roldan, Eugenia organization: Department of Infectious and Tropical Diseases, University of Brescia and ASST Spedali di Brescia, Brescia, Italy – sequence: 78 givenname: Camillo surname: Rossi fullname: Rossi, Camillo organization: Direzione Sanitaria, ASST Spedali Civili di Brescia, Brescia, Italy – sequence: 79 givenname: Riccardo orcidid: 0000-0003-0029-9383 surname: Castagnoli fullname: Castagnoli, Riccardo organization: Department of Pediatrics, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy – sequence: 80 givenname: Daniela surname: Montagna fullname: Montagna, Daniela organization: Laboratory of Immunology and Transplantation, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy., Department of Clinical, Surgical, Diagnostic and Pediatric Sciences, University of Pavia, Pavia, Italy – sequence: 81 givenname: Amelia orcidid: 0000-0002-1773-6482 surname: Licari fullname: Licari, Amelia organization: Department of Pediatrics, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy – sequence: 82 givenname: Gian Luigi surname: Marseglia fullname: Marseglia, Gian Luigi organization: Department of Pediatrics, Fondazione IRCCS Policlinico San Matteo, University of Pavia, Pavia, Italy – sequence: 83 givenname: Xavier surname: Duval fullname: Duval, Xavier organization: INSERM CIC 1425, Paris, France., AP-HP, University Hospital of Bichat, Paris, France., University Paris Diderot, Paris 7, UFR de Médecine-Bichat, Paris, France., Infection, Antimicrobials, Modelling, Evolution (IAME), INSERM, UMRS1137, University of Paris, Paris, France., AP-HP, Bichat Claude Bernard Hospital, Infectious and Tropical Diseases Department, Paris, France – sequence: 84 givenname: Jade surname: Ghosn fullname: Ghosn, Jade organization: Infection, Antimicrobials, Modelling, Evolution (IAME), INSERM, UMRS1137, University of Paris, Paris, France., AP-HP, Bichat Claude Bernard Hospital, Infectious and Tropical Diseases Department, Paris, France – sequence: 85 givenname: John S. orcidid: 0000-0003-3186-3047 surname: Tsang fullname: Tsang, John S. organization: Center for Human Immunology, NIH, Bethesda, MD, USA., Multiscale Systems Biology Section, Laboratory of Immune System Biology, NIAID, NIH, Bethesda, MD, USA – sequence: 86 givenname: Raphaela orcidid: 0000-0001-7865-5769 surname: Goldbach-Mansky fullname: Goldbach-Mansky, Raphaela organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 87 givenname: Kai orcidid: 0000-0002-5426-4648 surname: Kisand fullname: Kisand, Kai organization: Institute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia – sequence: 88 givenname: Michail S. surname: Lionakis fullname: Lionakis, Michail S. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 89 givenname: Anne orcidid: 0000-0003-2603-0323 surname: Puel fullname: Puel, Anne organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 90 givenname: Shen-Ying surname: Zhang fullname: Zhang, Shen-Ying organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 91 givenname: Steven M. orcidid: 0000-0003-3207-5464 surname: Holland fullname: Holland, Steven M. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 92 givenname: Guy surname: Gorochov fullname: Gorochov, Guy organization: Sorbonne Université, INSERM, Centre d’Immunologie et des Maladies Infectieuses, (CIMI-Paris), Paris, France., Département d’Immunologie, AP-HP, Hôpital Pitié-Salpétrière, Paris, France – sequence: 93 givenname: Emmanuelle orcidid: 0000-0002-7358-9157 surname: Jouanguy fullname: Jouanguy, Emmanuelle organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 94 givenname: Charles M. surname: Rice fullname: Rice, Charles M. organization: Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA – sequence: 95 givenname: Aurélie orcidid: 0000-0001-7209-6257 surname: Cobat fullname: Cobat, Aurélie organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 96 givenname: Luigi D. orcidid: 0000-0002-8335-0262 surname: Notarangelo fullname: Notarangelo, Luigi D. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 97 givenname: Laurent orcidid: 0000-0001-7016-6493 surname: Abel fullname: Abel, Laurent organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA – sequence: 98 givenname: Helen C. orcidid: 0000-0002-5582-9110 surname: Su fullname: Su, Helen C. organization: Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD, USA – sequence: 99 givenname: Jean-Laurent orcidid: 0000-0002-7782-4169 surname: Casanova fullname: Casanova, Jean-Laurent organization: Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Necker Hospital for Sick Children, Paris, France., University of Paris, Imagine Institute, Paris, France., St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA., Howard Hughes Medical Institute, New York, NY, USA., Pediatric Hematology and Immunology Unit, Necker Hospital for Sick Children, AP-HP, Paris, France – sequence: 100 givenname: Andrés Augusto surname: Arias fullname: Arias, Andrés Augusto |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32972996$$D View this record in MEDLINE/PubMed https://pasteur.hal.science/pasteur-02958871$$DView record in HAL http://kipublications.ki.se/Default.aspx?queryparsed=id:144930113$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Contributor | Corsico, Angelo G Ogishi, Masato Castelle, Martin Dehban, Amin Delplancq, Geoffroy Carrabba, Maria Blanchard-Rohner, Geraldine Colkesen, Fatih Koroleva, Galina Stack, Michael Liu, Hui Boisson, Bertrand Bajolle, Fanny Papandrea, Dominick Liu, Dana Bloomfield, Marketa Darley, David Ross Arslan, Sevket Clavé, Père Dauby, Nicolas Aguilera-Albesa, Sergio Rapaport, Franck Kashyap, Anuj Abad, Jorge Allende, Luis M de Vera, Martín Castillo Castro, Mateus V Snow, Andrew L Dalmau, David Zhang, Peng Boucherit, Soraya Kochetkov, Tatiana Boyarchuk, Oksana Amador-Borrero, Blanca Beurton, Alexandra Amoura, Zahir Assant, Sophie Bueno, Maria Rita P Baldolli, Aurélie Roynard, Manon Calimli, Semra Darazam, Ilad Alavi Chauvin, Samuel D Cheng, Matthew P Bolivar-Prados, Mireia Ramos, Miquel Alfonso Bousfiha, Ahmed A Charbit, Bruno Ballester, Maite Feldman, Hagit Baris Castelli, Francesco Bosticardo, Marita Auguet, Terese Ochoa, Sebastian Chbihi, Marwa Azot, Axelle Clotet, Bonaventura Nadji, Seyed Alireza Vladikine, Natasha Casasnovas, Carlos de Pontual, Loic Bouvatti |
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| Copyright | Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works Attribution Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works 2020 The Authors |
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| License | https://creativecommons.org/licenses/by/4.0 Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Attribution: http://creativecommons.org/licenses/by This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
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| Snippet | The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs). Individuals that lack specific IFNs... Interindividual clinical variability in the course of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is vast. We report that at least... The genetics underlying severe COVID-19The immune system is complex and involves many genes, including those that encode cytokines known as interferons (IFNs).... |
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| SubjectTerms | Adult Aged Aged, 80 and over Antibodies, Neutralizing Antibodies, Neutralizing - blood Antiviral drugs Asymptomatic Asymptomatic Infections Autoantibodies Autoantibodies - blood Autoimmunity Betacoronavirus Case-Control Studies Control Groups Coronaviridae Coronavirus Infections Coronavirus Infections - immunology Coronaviruses COVID-19 Critical Illness Cytokines Disease Female Genetics Humans Immune system Immunoglobulin G Immunoglobulin G - blood Immunoglobulins Immunology Infections Infectious diseases Interferon alpha-2 Interferon alpha-2 - immunology Interferon Type I Interferon Type I - immunology Life Sciences Male Males Middle Aged Mutation Online Pandemics Patients Pneumonia Pneumonia, Viral Pneumonia, Viral - immunology Public health Respiratory diseases Risk factors SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Viral infections |
| Title | Autoantibodies against type I IFNs in patients with life-threatening COVID-19 |
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