IgG Anti-Spike Antibodies and Surrogate Neutralizing Antibody Levels Decline Faster 3 to 10 Months After BNT162b2 Vaccination Than After SARS-CoV-2 Infection in Healthcare Workers.


Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2022
Historique:
received: 31 03 2022
accepted: 16 05 2022
entrez: 5 7 2022
pubmed: 6 7 2022
medline: 7 7 2022
Statut: epublish

Résumé

IgG anti-spike (S) antibodies arise after SARS-CoV-2 infection as well as vaccination. Levels of IgG anti-S are linked to neutralizing antibody titers and protection against (re)infection. We measured IgG anti-S and surrogate neutralizing antibody kinetics against Wild Type (WT) and 4 Variants of Concern (VOC) in health care workers (HCW) 3 and 10 months after natural infection ("infection", n=83) or vaccination (2 doses of BNT162b2) with ("hybrid immunity", n=17) or without prior SARS-CoV-2 infection ("vaccination", n=97). The humoral immune response in the "vaccination" cohort was higher at 3 months, but lower at 10 months, compared to the "infection" cohort due to a faster decline. The "hybrid immunity" cohort had the highest antibody levels at 3 and 10 months with a slower decline compared to the "vaccination" cohort. Surrogate neutralizing antibody levels (expressed as %inhibition of ACE-2 binding) showed a linear relation with log10 of IgG anti-S against WT and four VOC. IgG anti-S corresponding to 90% inhibition ranged from 489 BAU/mL for WT to 1756 BAU/mL for Beta variant. Broad pseudoneutralization predicted live virus neutralization of Omicron BA.1 in 20 randomly selected high titer samples. Hybrid immunity resulted in the strongest humoral immune response. Antibodies induced by natural infection decreased more slowly than after vaccination, resulting in higher antibody levels at 10 months compared to vaccinated HCW without prior infection. There was a linear relationship between surrogate neutralizing activity and log10 IgG anti-S for WT and 4 VOC, although some VOC showed reduced sensitivity to pseudoneutralization.

Sections du résumé

Background
IgG anti-spike (S) antibodies arise after SARS-CoV-2 infection as well as vaccination. Levels of IgG anti-S are linked to neutralizing antibody titers and protection against (re)infection.
Methods
We measured IgG anti-S and surrogate neutralizing antibody kinetics against Wild Type (WT) and 4 Variants of Concern (VOC) in health care workers (HCW) 3 and 10 months after natural infection ("infection", n=83) or vaccination (2 doses of BNT162b2) with ("hybrid immunity", n=17) or without prior SARS-CoV-2 infection ("vaccination", n=97).
Results
The humoral immune response in the "vaccination" cohort was higher at 3 months, but lower at 10 months, compared to the "infection" cohort due to a faster decline. The "hybrid immunity" cohort had the highest antibody levels at 3 and 10 months with a slower decline compared to the "vaccination" cohort. Surrogate neutralizing antibody levels (expressed as %inhibition of ACE-2 binding) showed a linear relation with log10 of IgG anti-S against WT and four VOC. IgG anti-S corresponding to 90% inhibition ranged from 489 BAU/mL for WT to 1756 BAU/mL for Beta variant. Broad pseudoneutralization predicted live virus neutralization of Omicron BA.1 in 20 randomly selected high titer samples.
Conclusions
Hybrid immunity resulted in the strongest humoral immune response. Antibodies induced by natural infection decreased more slowly than after vaccination, resulting in higher antibody levels at 10 months compared to vaccinated HCW without prior infection. There was a linear relationship between surrogate neutralizing activity and log10 IgG anti-S for WT and 4 VOC, although some VOC showed reduced sensitivity to pseudoneutralization.

Identifiants

pubmed: 35784321
doi: 10.3389/fimmu.2022.909910
pmc: PMC9241488
doi:

Substances chimiques

Antibodies, Neutralizing 0
Antibodies, Viral 0
Immunoglobulin G 0
BNT162 Vaccine N38TVC63NU

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

909910

Commentaires et corrections

Type : ErratumIn

Informations de copyright

Copyright © 2022 Decru, Van Elslande, Steels, Van Pottelbergh, Godderis, Van Holm, Bossuyt, Van Weyenbergh, Maes and Vermeersch.

Déclaration de conflit d'intérêts

PV reports personal fees from Roche, outside the submitted work. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Bram Decru (B)

University Hospitals Leuven, Clinical Department of Laboratory Medicine and National Reference Center for Respiratory Pathogens, Leuven, Belgium.

Jan Van Elslande (J)

University Hospitals Leuven, Clinical Department of Laboratory Medicine and National Reference Center for Respiratory Pathogens, Leuven, Belgium.

Sophie Steels (S)

University Hospitals Leuven, Clinical Department of Laboratory Medicine and National Reference Center for Respiratory Pathogens, Leuven, Belgium.

Gijs Van Pottelbergh (G)

Academic Centre of General Practice, KU Leuven, Leuven, Belgium.
Department of Public Health and Primary Care, KU Leuven, Leuven, Belgium.

Lode Godderis (L)

Academic Centre of General Practice, KU Leuven, Leuven, Belgium.
Department of Public Health and Primary Care, KU Leuven, Leuven, Belgium.
Environment and Health, Department of Public Health and Primary Care, KU Leuven, Leuven, Belgium.
Group IDEWE, External Service for Prevention and Protection at Work, Heverlee, Belgium.

Bram Van Holm (B)

Laboratory of Clinical and Epidemiological Virology, Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.

Xavier Bossuyt (X)

University Hospitals Leuven, Clinical Department of Laboratory Medicine and National Reference Center for Respiratory Pathogens, Leuven, Belgium.

Johan Van Weyenbergh (J)

Laboratory of Clinical and Epidemiological Virology, Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.

Piet Maes (P)

Laboratory of Clinical and Epidemiological Virology, Department of Microbiology, Immunology and Transplantation, Rega Institute, KU Leuven, Leuven, Belgium.

Pieter Vermeersch (P)

University Hospitals Leuven, Clinical Department of Laboratory Medicine and National Reference Center for Respiratory Pathogens, Leuven, Belgium.
Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium.

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