Abstract
Background: The development of vaccine candidates for COVID-19, and the administration of booster vaccines, has meant a significant reduction in COVID-19 related deaths world-wide and the easing of global restrictions. However, new variants of SARS-CoV-2 have emerged with less susceptibility to vaccine induced immunity leading to breakthrough infections among vaccinated people. It is generally acknowledged that immunoglobulins play the major role in immune-protection, primarily through binding to the SARS-COV-2 receptor binding domain (RBD) and thereby inhibiting viral binding to the ACE2 receptor. However, there are limited investigations of anti-RBD isotypes (IgM, IgG, IgA) and IgG subclasses (IgG1–4) over the course of vaccination and breakthrough infection. Method: In this study, SARS-CoV-2 humoral immunity is examined in a single subject with unique longitudinal sampling. Over a two year period, the subject received three doses of vaccine, had two active breakthrough infections and 22 blood samples collected. Serological testing included anti-nucleocapsid total antibodies, anti-RBD total antibodies, IgG, IgA, IgM and IgG subclasses, neutralization and ACE2 inhibition against the wildtype (WT), Delta and Omicron variants. Results: Vaccination and breakthrough infections induced IgG, specifically IgG1 and IgG4 as well as IgM and IgA. IgG1 and IgG4 responses were cross reactive and associated with broad inhibition. Conclusion: The findings here provide novel insights into humoral immune response characteristics associated with SARS-CoV-2 breakthrough infections.
Original language | English |
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Article number | e910 |
Journal | Immunity, Inflammation and Disease |
Volume | 11 |
Issue number | 6 |
ISSN | 2050-4527 |
DOIs | |
Publication status | Published - 2023 |
Bibliographical note
Publisher Copyright:© 2023 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.
Keywords
- antibody
- antibody isotypes
- antibody subclasses
- case report
- COVID-19
- humoral immunity
- IgG
- SARS-CoV-2