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Letter
Third COVID-19 vaccine dose with BNT162b2 in patients with ANCA-associated vasculitis
  1. Claudius Speer1,2,
  2. Maximilian Töllner1,
  3. Louise Benning1,
  4. Katrin Klein1,
  5. Marie Bartenschlager3,
  6. Christian Nusshag1,
  7. Florian Kälble1,
  8. Paula Reichel1,
  9. Paul Schnitzler3,
  10. Martin Zeier1,
  11. Christian Morath1,
  12. Wilhelm H Schmitt4,
  13. Raoul Bergner5,
  14. Ralf Bartenschlager3,6,
  15. Matthias Schaier1
  1. 1 Nephrology, University Hospital Heidelberg, Heidelberg, Germany
  2. 2 Molecular Medicine Partnership Unit Heidelberg, European Molecular Biology Laboratory, Heidelberg, Baden-Württemberg, Germany
  3. 3 Department of Infectious Diseases, Virology Heidelberg, Heidelberg, Germany
  4. 4 Department of Nephrology and Rheumatology, Kidney Center Weinheim, Weinheim, Germany
  5. 5 Department of Internal Medicine A, Clinical Center Ludwigshafen, Ludwigshafen, Germany
  6. 6 Division of Virus-Associated Carcinogenesis, German Cancer Research Centre, Heidelberg, Baden-Württemberg, Germany
  1. Correspondence to Dr Claudius Speer, Nephrology, University Hospital Heidelberg, Heidelberg, Germany; claudius.speer{at}med.uni-heidelberg.de

https://doi.org/10.1136/annrheumdis-2021-221747

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    Humoral and cellular immune responses after standard two-dose COVID-19 vaccination are reduced in immunosuppressed patients with antineutrophil cytoplasmic antibodies associated vasculitis (AAV).1–3 Emerging variants such as B.1.617.2 (delta) are of particular concern because of their higher transmissibility and partial immune escape.4 AAV patients with lower neutralising antibody levels may become particularly susceptible to these variants of concern and additional booster vaccination may be required.

    We performed a prospective observational study at three different German vasculitis centres to investigate humoral responses against the variant of concern B.1.617.2 after a third vaccine dose with BNT162b2 in 21 patients with AAV on immunosuppressive maintenance therapy. All individuals met the 2017 provisional American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) criteria for AAV. We investigated antispike S1 IgG and surrogate neutralising antibodies a median (IQR) of 23 (21–58) days after standard two-dose COVID-19 vaccination, immediately before a third vaccine dose, as well as a median (IQR) of 21 (21–21) days after third vaccination (online supplemental material). The third vaccine dose was administered a median (IQR) of 103 (72–126) days after second vaccination. In addition, neutralisation activity against B.1.617.2 was analysed in vitro in SARS-CoV-2-infected VeroE6 cells after second vaccination and before and after the third vaccine dose (online supplemental methods).5 Patients were also stratified according to whether or not they had received rituximab treatment as maintenance therapy in the last year. Baseline characteristics and individual immunosuppressive regimens are given in (online supplemental tables S1 and S2).

    Supplemental material

    [annrheumdis-2021-221747supp001.pdf]

    After second COVID-19 vaccine dose, the median (IQR) anti-S1 IgG index was 1.6 (0.1–3.0) and the median (IQR) per cent inhibition of surrogate neutralising antibodies 34 (31–70; figure 1A). A median (IQR) of 103 (72–126) days after the second vaccine dose, both anti-S1 IgG and neutralising surrogate antibodies decreased …

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors Contributed to the manuscript by planning the study: CS, LB, KK and MS, performed the experiments and collected the data: CS, MT, LB, MB, CN, FK, PR and PS, analysis and interpretation of data: CS, MT, LB, PS, CM and MS and preparation and revision of the manuscript: CS, MT, LB, PR, MZ, CM, WHS, RBergner, RBartenschlager and MS. All authors contributed to the article and approved the submitted version.

    • Funding Funding for this study has been received from Dietmar Hopp Stiftung. CS was funded by the Physician Scientist Program of the Heidelberg Faculty of Medicine. LB was funded by the Rahel Goitein-Strauss Program of the Heidelberg Faculty of Medicine. RBartenschlager was supported by the program for surveillance and control of SARS-CoV-2 mutations of the State of Baden-Württemberg, the German Federal Research Network Applied Surveillance and Testing (BFAST) within the Network University Medicine, the DKFZ@fightCOVID initiative and the Helmholtz Association’s Initiative and Networking Fund Project ‘Virological and immunological determinants of COVID-19 pathogenesis—lessons to get prepared for future pandemics (KA1-Co-02 ‘COVIPA’)’.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.