Evidence map›Paper›PMID 35143756›Full record

ArticleCell reports2022

B cell receptor repertoire kinetics after SARS-CoV-2 infection and vaccination.

Prasanti Kotagiri, Federica Mescia, William M Rae, Laura Bergamaschi, Zewen K Tuong, Lorinda Turner, Kelvin Hunter, Pehuén P Gerber, Myra Hosmillo, Cambridge Institute of Therapeutic Immunology and Infectious Disease-National Institute of Health Research (CITIID-NIHR) COVID BioResource Collaboration and 11 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 58 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors at 4 institutions in 3 countries.

Prasanti KotagiriCambridge 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.
Federica MesciaCambridge 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.
William M RaeCambridge 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.
Laura BergamaschiCambridge 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.
Zewen K TuongDepartment of Medicine, University of Cambridge School of Clinical Medicine, Cambridge CB2 0QQ, UK; Cellular Genetics, Wellcome Sanger Institute, Hinxton, Cambridge CB10 1RQ, UK.
Lorinda TurnerCambridge 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.
Kelvin HunterCambridge 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.
Pehuén P GerberCambridge 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.
Myra HosmilloDivision of Virology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Cambridge Institute of Therapeutic Immunology and Infectious Disease-National Institute of Health Research (CITIID-NIHR) COVID BioResource Collaboration
Christoph HessCambridge 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 University Hospital Basel, Basel 4031, Switzerland; Botnar Research Centre for Child Health (BRCCH) University Basel and ETH Zurich, Basel 4059, Switzerland.
Menna R ClatworthyCambridge 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, Hinxton, Cambridge CB10 1RQ, UK.
Ian G GoodfellowDivision of Virology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK.
Nicholas J MathesonCambridge 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.
Eoin F McKinneyCambridge 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.
Mark R WillsCambridge 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.
Ravindra K GuptaCambridge 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.
John R BradleyDepartment 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.
Rachael J M Bashford-RogersNuffield Department of Medicine, Wellcome Centre for Human Genetics, Oxford OX3 7BN, UK.
Paul A LyonsCambridge 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.
Kenneth G C SmithCambridge 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.
University of Cambridge · GBCentre for Human Genetics · GBNHS Blood and Transplant · GBWellcome/MRC Cambridge Stem Cell Institute · GB

Funding

Department of HealthMedical Research Council MR/P008801/1Medical Research Council MR/S035842/1Medical Research Council MR/V028448/1Medical Research Council MR/W018861/1Wellcome Trust 200871/Z/16/ZWellcome Trust 207498/Z/17/Z
6 · The paper itself

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.

Indexed as

VaccinationB-LymphocytesBNT162 VaccineClonal EvolutionCOVID-19HumansImmunoglobulin Heavy ChainsImmunoglobulin IsotypesImmunoglobulin Variable RegionKineticsReceptors, Antigen, B-CellSARS-CoV-2Severity of Illness IndexSomatic Hypermutation, ImmunoglobulinSpike Glycoprotein, CoronavirusBNT162 VaccineImmunoglobulin Heavy ChainsImmunoglobulin IsotypesImmunoglobulin Variable RegionReceptors, Antigen, B-CellSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2B cell receptor repertoireCOVID-19SARS-CoV-2 vaccination

Identifiers

PMID35143756
PMCPMC8801326
OpenAlexW4221047175

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.