Reduced antibody cross-reactivity following infection with B.1.1.7 than with parental SARS-CoV-2 strains

  1. Nikhil Faulkner
  2. Kevin W Ng
  3. Mary Y Wu
  4. Ruth Harvey
  5. Marios Margaritis
  6. Stavroula Paraskevopoulou
  7. Catherine Houlihan
  8. Saira Hussain
  9. Maria Greco
  10. William Bolland
  11. Scott Warchal
  12. Judith Heaney
  13. Hannah Rickman
  14. Moria Spyer
  15. Daniel Frampton
  16. Matthew Byott
  17. Tulio de Oliveira
  18. Alex Sigal
  19. Svend Kjaer
  20. Charles Swanton
  21. Sonia Gandhi
  22. Rupert Beale
  23. Steve j Gamblin
  24. John W McCauley
  25. Rodney Stuart Daniels
  26. Michael Howell
  27. David Bauer
  28. Eleni Nastouli
  29. SAFER Investigators
  30. George Kassiotis  Is a corresponding author
  1. The Francis Crick Institute, United Kingdom
  2. University College London, United Kingdom
  3. University College London Hospital, United Kingdom
  4. University of KwaZulu-Natal,SA, South Africa
  5. Africa Health Research Institute, University of KwaZulu-Natal, South Africa
  6. The Francis Crick Insitute, United Kingdom

Abstract

Background: The degree of heterotypic immunity induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains is a major determinant of the spread of emerging variants and the success of vaccination campaigns, but remains incompletely understood.

Methods: We examined the immunogenicity of SARS-CoV-2 variant B.1.1.7 (Alpha) that arose in the United Kingdom and spread globally. We determined titres of spike glycoprotein-binding antibodies and authentic virus neutralising antibodies induced by B.1.1.7 infection to infer homotypic and heterotypic immunity.

Results: Antibodies elicited by B.1.1.7 infection exhibited significantly reduced recognition and neutralisation of parental strains or of the South Africa variant B.1.351 (Beta) than of the infecting variant. The drop in cross-reactivity was significantly more pronounced following B.1.1.7 than parental strain infection.

Conclusions: The results indicate that heterotypic immunity induced by SARS-CoV-2 variants is asymmetric.

Data availability

All data generated or analysed during this study are included in the manuscript and supporting files.

Article and author information

Author details

  1. Nikhil Faulkner

    Retroviral Immunology, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  2. Kevin W Ng

    Retroviral Immunology, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-1635-6768
  3. Mary Y Wu

    High Throughput Screening STP, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2074-6171
  4. Ruth Harvey

    Worldwide Influenza Centre, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Marios Margaritis

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  6. Stavroula Paraskevopoulou

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  7. Catherine Houlihan

    University College London Hospital, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  8. Saira Hussain

    RNA Virus Replication Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  9. Maria Greco

    RNA Virus Replication Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  10. William Bolland

    Retroviral Immunology, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  11. Scott Warchal

    High Throughput Screening STP, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  12. Judith Heaney

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  13. Hannah Rickman

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  14. Moria Spyer

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  15. Daniel Frampton

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  16. Matthew Byott

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  17. Tulio de Oliveira

    School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal,SA, Durban, South Africa
    Competing interests
    The authors declare that no competing interests exist.
  18. Alex Sigal

    School of Laboratory Medicine and Medical Sciences, Africa Health Research Institute, University of KwaZulu-Natal, Durban, South Africa
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8571-2004
  19. Svend Kjaer

    Structural Biology, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9767-8683
  20. Charles Swanton

    Structural Biology, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  21. Sonia Gandhi

    Neurodegradation Biology Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  22. Rupert Beale

    Cell Biology of Infection Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6705-8560
  23. Steve j Gamblin

    Cell Biology of Infection Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  24. John W McCauley

    Worldwide Influenza Centre, The Francis Crick Insitute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-4744-6347
  25. Rodney Stuart Daniels

    Worldwide Influenza Centre, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  26. Michael Howell

    High Throughput Screening, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  27. David Bauer

    RNA Virus Replication Laboratory, The Francis Crick Institute, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  28. Eleni Nastouli

    Advanced Pathogen Diagnostics, University College London, London, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  29. SAFER Investigators

  30. George Kassiotis

    Retroviral Immunology, The Francis Crick Institute, London, United Kingdom
    For correspondence
    george.kassiotis@crick.ac.uk
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-8457-2633

Funding

Francis Crick Institute

  • Nikhil Faulkner
  • Kevin W Ng
  • Mary Y Wu
  • Ruth Harvey
  • Saira Hussain
  • Maria Greco
  • William Bolland
  • Scott Warchal
  • Svend Kjaer
  • Charles Swanton
  • Sonia Gandhi
  • Rupert Beale
  • Steve j Gamblin
  • John W McCauley
  • Rodney Stuart Daniels
  • Michael Howell
  • David Bauer
  • George Kassiotis

Max Planck Institute for Dynamics of Complex Technical Systems Magdeburg

  • Alex Sigal

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Human subjects: Serum or plasma samples were obtained from University College London Hospitals (UCLH) (REC ref: 20/HRA/2505).

Copyright

© 2021, Faulkner et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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  1. Nikhil Faulkner
  2. Kevin W Ng
  3. Mary Y Wu
  4. Ruth Harvey
  5. Marios Margaritis
  6. Stavroula Paraskevopoulou
  7. Catherine Houlihan
  8. Saira Hussain
  9. Maria Greco
  10. William Bolland
  11. Scott Warchal
  12. Judith Heaney
  13. Hannah Rickman
  14. Moria Spyer
  15. Daniel Frampton
  16. Matthew Byott
  17. Tulio de Oliveira
  18. Alex Sigal
  19. Svend Kjaer
  20. Charles Swanton
  21. Sonia Gandhi
  22. Rupert Beale
  23. Steve j Gamblin
  24. John W McCauley
  25. Rodney Stuart Daniels
  26. Michael Howell
  27. David Bauer
  28. Eleni Nastouli
  29. SAFER Investigators
  30. George Kassiotis
(2021)
Reduced antibody cross-reactivity following infection with B.1.1.7 than with parental SARS-CoV-2 strains
eLife 10:e69317.
https://doi.org/10.7554/eLife.69317

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https://doi.org/10.7554/eLife.69317

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