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B cell receptor repertoire kinetics after SARS-CoV-2 infection and vaccination.
Kotagiri, Prasanti; Mescia, Federica; Rae, William M; Bergamaschi, Laura; Tuong, Zewen K; Turner, Lorinda; Hunter, Kelvin; Gerber, Pehuén P; Hosmillo, Myra; Hess, Christoph; Clatworthy, Menna R; Goodfellow, Ian G; Matheson, Nicholas J; McKinney, Eoin F; Wills, Mark R; Gupta, Ravindra K; Bradley, John R; Bashford-Rogers, Rachael J M; Lyons, Paul A; Smith, Kenneth G C.
  • Kotagiri P; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK. Electronic address: pk488@cam.ac.uk.
  • Mescia F; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Rae WM; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Bergamaschi L; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Tuong ZK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; Cellular Genetics, Wellcome Sanger Institute, Hinxton, Cambridge CB10 1RQ, UK.
  • Turner L; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Hunter K; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Gerber PP; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Hosmillo M; Division of Virology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
  • Hess C; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; Department of Biomedicine, University and Univers
  • Clatworthy MR; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; Cellular Genetics, Wellcome Sanger Institute, Hin
  • Goodfellow IG; Division of Virology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
  • Matheson NJ; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; NHS Blood and Transplant, Cambridge CB2 1PT, UK.
  • McKinney EF; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Wills MR; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Gupta RK; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK.
  • Bradley JR; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; NIHR BioResource, Cambridge University Hospitals NHS Foundation, Cambridge Biomedical Campus, Cambridge CB2 0QQ, UK.
  • Bashford-Rogers RJM; Nuffield Department of Medicine, Wellcome Centre for Human Genetics, Oxford OX3 7BN, UK.
  • Lyons PA; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK. Electronic address: pal34@cam.ac.uk.
  • Smith KGC; Cambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK; Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK. Electronic address: kgcs2@cam.ac.uk.
Cell Rep ; 38(7): 110393, 2022 02 15.
Article in English | MEDLINE | ID: covidwho-1719435
ABSTRACT
B cells are important in immunity to both severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and vaccination, but B cell receptor (BCR) repertoire development in these contexts has not been compared. We analyze serial samples from 171 SARS-CoV-2-infected individuals and 63 vaccine recipients and find the global BCR repertoire differs between them. Following infection, immunoglobulin (Ig)G1/3 and IgA1 BCRs increase, somatic hypermutation (SHM) decreases, and, in severe disease, IgM and IgA clones are expanded. In contrast, after vaccination, the proportion of IgD/M BCRs increase, SHM is unchanged, and expansion of IgG clones is prominent. VH1-24, which targets the N-terminal domain (NTD) and contributes to neutralization, is expanded post infection except in the most severe disease. Infection generates a broad distribution of SARS-CoV-2-specific clones predicted to target the spike protein, while a more focused response after vaccination mainly targets the spike's receptor-binding domain. Thus, the nature of SARS-CoV-2 exposure differentially affects BCR repertoire development, potentially informing vaccine strategies.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Receptors, Antigen, B-Cell / Vaccination / COVID-19 Type of study: Prognostic study Topics: Vaccines Limits: Humans Language: English Journal: Cell Rep Year: 2022 Document Type: Article

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Receptors, Antigen, B-Cell / Vaccination / COVID-19 Type of study: Prognostic study Topics: Vaccines Limits: Humans Language: English Journal: Cell Rep Year: 2022 Document Type: Article