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Fatal COVID-19 outcomes are associated with an antibody response targeting epitopes shared with endemic coronaviruses.
McNaughton, Anna L; Paton, Robert S; Edmans, Matthew; Youngs, Jonathan; Wellens, Judith; Phalora, Prabhjeet; Fyfe, Alex; Belij-Rammerstorfer, Sandra; Bolton, Jai S; Ball, Jonathan; Carnell, George W; Dejnirattisai, Wanwisa; Dold, Christina; Eyre, David W; Hopkins, Philip; Howarth, Alison; Kooblall, Kreepa; Klim, Hannah; Leaver, Susannah; Lee, Lian Ni; López-Camacho, César; Lumley, Sheila F; Macallan, Derek C; Mentzer, Alexander J; Provine, Nicholas M; Ratcliff, Jeremy; Slon-Compos, Jose; Skelly, Donal; Stolle, Lucas; Supasa, Piyada; Temperton, Nigel; Walker, Chris; Wang, Beibei; Wyncoll, Duncan; Simmonds, Peter; Lambe, Teresa; Baillie, John Kenneth; Semple, Malcolm G; Openshaw, Peter Jm; Obolski, Uri; Turner, Marc; Carroll, Miles; Mongkolsapaya, Juthathip; Screaton, Gavin; Kennedy, Stephen H; Jarvis, Lisa; Barnes, Eleanor; Dunachie, Susanna; Lourenço, José; Matthews, Philippa C.
  • McNaughton AL; Peter Medawar Building for Pathogen Research.
  • Paton RS; Nuffield Department of Medicine, and.
  • Edmans M; Peter Medawar Building for Pathogen Research.
  • Youngs J; Department of Zoology, University of Oxford, Oxford, United Kingdom.
  • Wellens J; Peter Medawar Building for Pathogen Research.
  • Phalora P; Nuffield Department of Medicine, and.
  • Fyfe A; Department of Zoology, University of Oxford, Oxford, United Kingdom.
  • Belij-Rammerstorfer S; Institute of Infection & Immunity, St George's University of London, London, United Kingdom.
  • Bolton JS; Peter Medawar Building for Pathogen Research.
  • Ball J; Translational Gastroenterology Unit, Experimental Medicine Division, Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
  • Carnell GW; Translational Research for Gastrointestinal Diseases, University Hospitals Leuven, Leuven, Belgium.
  • Dejnirattisai W; Peter Medawar Building for Pathogen Research.
  • Dold C; Nuffield Department of Medicine, and.
  • Eyre DW; Peter Medawar Building for Pathogen Research.
  • Hopkins P; Department of Zoology, University of Oxford, Oxford, United Kingdom.
  • Howarth A; The Jenner Institute Laboratories, University of Oxford, Oxford, United Kingdom.
  • Kooblall K; Peter Medawar Building for Pathogen Research.
  • Klim H; Department of Zoology, University of Oxford, Oxford, United Kingdom.
  • Leaver S; General Intensive Care service, St George's University Hospital National Health Service (NHS) Trust, London, United Kingdom.
  • Lee LN; Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom.
  • López-Camacho C; Wellcome Centre for Human Genetics, Nuffield Department of Medicine.
  • Lumley SF; Oxford Vaccine Group, Department of Paediatrics, and.
  • Macallan DC; Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.
  • Mentzer AJ; Centre for Human & Applied Physiological Sciences, School of Basic & Medical Biosciences, Faculty of Life Sciences & Medicine, King's College, London, United Kingdom.
  • Provine NM; Department of Microbiology/Infectious Diseases, Oxford University Hospitals NHS Foundation Trust, John Radcliffe Hospital, Oxford, United Kingdom.
  • Ratcliff J; Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, and.
  • Slon-Compos J; Peter Medawar Building for Pathogen Research.
  • Skelly D; Department of Zoology, University of Oxford, Oxford, United Kingdom.
  • Stolle L; Future of Humanity Institute, Department of Philosophy, and.
  • Supasa P; General Intensive Care service, St George's University Hospital National Health Service (NHS) Trust, London, United Kingdom.
  • Temperton N; Peter Medawar Building for Pathogen Research.
  • Walker C; Nuffield Department of Medicine, and.
  • Wang B; Wellcome Centre for Human Genetics, Nuffield Department of Medicine.
  • Wyncoll D; Peter Medawar Building for Pathogen Research.
  • Simmonds P; Institute of Infection & Immunity, St George's University of London, London, United Kingdom.
  • Lambe T; Wellcome Centre for Human Genetics, Nuffield Department of Medicine.
  • Baillie JK; Translational Gastroenterology Unit, Experimental Medicine Division, Nuffield Department of Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
  • Semple MG; Peter Medawar Building for Pathogen Research.
  • Openshaw PJ; Nuffield Department of Medicine, and.
  • Obolski U; Peter Medawar Building for Pathogen Research.
  • Turner M; Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom.
  • Carroll M; Oxford University Hospitals NHS Foundation Trust, Oxford, United Kingdom.
  • Mongkolsapaya J; Department of Biochemistry, University of Oxford, Oxford, United Kingdom.
  • Screaton G; Wellcome Centre for Human Genetics, Nuffield Department of Medicine.
  • Kennedy SH; Viral Pseudotype Unit, Medway School of Pharmacy, University of Kent, Chatham, United Kingdom.
  • Jarvis L; Meso Scale Diagnostics, Rockville, Maryland, USA.
  • Barnes E; Wellcome Centre for Human Genetics, Nuffield Department of Medicine.
  • Dunachie S; Intensive Care Medicine, Guy's and St Thomas' Hospital NHS Foundation Trust, London, United Kingdom.
JCI Insight ; 7(13)2022 07 08.
Article in English | MEDLINE | ID: covidwho-1861743
ABSTRACT
The role of immune responses to previously seen endemic coronavirus epitopes in severe acute respiratory coronavirus 2 (SARS-CoV-2) infection and disease progression has not yet been determined. Here, we show that a key characteristic of fatal outcomes with coronavirus disease 2019 (COVID-19) is that the immune response to the SARS-CoV-2 spike protein is enriched for antibodies directed against epitopes shared with endemic beta-coronaviruses and has a lower proportion of antibodies targeting the more protective variable regions of the spike. The magnitude of antibody responses to the SARS-CoV-2 full-length spike protein, its domains and subunits, and the SARS-CoV-2 nucleocapsid also correlated strongly with responses to the endemic beta-coronavirus spike proteins in individuals admitted to an intensive care unit (ICU) with fatal COVID-19 outcomes, but not in individuals with nonfatal outcomes. This correlation was found to be due to the antibody response directed at the S2 subunit of the SARS-CoV-2 spike protein, which has the highest degree of conservation between the beta-coronavirus spike proteins. Intriguingly, antibody responses to the less cross-reactive SARS-CoV-2 nucleocapsid were not significantly different in individuals who were admitted to an ICU with fatal and nonfatal outcomes, suggesting an antibody profile in individuals with fatal outcomes consistent with an "original antigenic sin" type response.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Spike Glycoprotein, Coronavirus / COVID-19 Type of study: Randomized controlled trials / Risk factors Limits: Humans Language: English Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Spike Glycoprotein, Coronavirus / COVID-19 Type of study: Randomized controlled trials / Risk factors Limits: Humans Language: English Year: 2022 Document Type: Article