Neutralisation sensitivity of the SARS-CoV-2 omicron (B.1.1.529) variant: a cross-sectional study.


Journal

The Lancet. Infectious diseases
ISSN: 1474-4457
Titre abrégé: Lancet Infect Dis
Pays: United States
ID NLM: 101130150

Informations de publication

Date de publication:
06 2022
Historique:
received: 18 12 2021
revised: 28 01 2022
accepted: 08 02 2022
pubmed: 21 3 2022
medline: 7 6 2022
entrez: 20 3 2022
Statut: ppublish

Résumé

The SARS-CoV-2 omicron (B.1.1.529) variant, which was first identified in November, 2021, spread rapidly in many countries, with a spike protein highly diverged from previously known variants, and raised concerns that this variant might evade neutralising antibody responses. We therefore aimed to characterise the sensitivity of the omicron variant to neutralisation. For this cross-sectional study, we cloned the sequence encoding the omicron spike protein from a diagnostic sample to establish an omicron pseudotyped virus neutralisation assay. We quantified the neutralising antibody ID Neutralising antibody responses in reference sample pools sampled shortly after infection or vaccination were substantially less potent against the omicron variant than against wild-type SARS-CoV-2 (seven-fold to 42-fold reduction in ID These data highlight the extensive, but incomplete, evasion of neutralising antibody responses by the omicron variant, and suggest that boosting with licensed vaccines might be sufficient to raise neutralising antibody titres to protective levels. European Union Horizon 2020 research and innovation programme, European and Developing Countries Clinical Trials Partnership, SciLifeLab, and the Erling-Persson Foundation.

Sections du résumé

BACKGROUND
The SARS-CoV-2 omicron (B.1.1.529) variant, which was first identified in November, 2021, spread rapidly in many countries, with a spike protein highly diverged from previously known variants, and raised concerns that this variant might evade neutralising antibody responses. We therefore aimed to characterise the sensitivity of the omicron variant to neutralisation.
METHODS
For this cross-sectional study, we cloned the sequence encoding the omicron spike protein from a diagnostic sample to establish an omicron pseudotyped virus neutralisation assay. We quantified the neutralising antibody ID
FINDINGS
Neutralising antibody responses in reference sample pools sampled shortly after infection or vaccination were substantially less potent against the omicron variant than against wild-type SARS-CoV-2 (seven-fold to 42-fold reduction in ID
INTERPRETATION
These data highlight the extensive, but incomplete, evasion of neutralising antibody responses by the omicron variant, and suggest that boosting with licensed vaccines might be sufficient to raise neutralising antibody titres to protective levels.
FUNDING
European Union Horizon 2020 research and innovation programme, European and Developing Countries Clinical Trials Partnership, SciLifeLab, and the Erling-Persson Foundation.

Identifiants

pubmed: 35305699
pii: S1473-3099(22)00129-3
doi: 10.1016/S1473-3099(22)00129-3
pmc: PMC8930016
pii:
doi:

Substances chimiques

Antibodies, Monoclonal 0
Antibodies, Monoclonal, Humanized 0
Antibodies, Neutralizing 0
Antibodies, Viral 0
COVID-19 Vaccines 0
Spike Glycoprotein, Coronavirus 0
spike protein, SARS-CoV-2 0
sotrovimab 1MTK0BPN8V
imdevimab 2Z3DQD2JHM
bamlanivimab 45I6OFJ8QH
casirivimab J0FI6WE1QN
etesevimab N7Q9NLF11I

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

813-820

Subventions

Organisme : Medical Research Council
ID : MR/W005611/1
Pays : United Kingdom

Informations de copyright

Copyright © 2022 Elsevier Ltd. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests STR is a cofounder of and held shares in deepCDR Biologics, which has been acquired by Alloy Therapeutics. DJS, GBKH, and BM have intellectual property rights associated with antibodies that neutralise the omicron variant. All other authors declare no competing interests.

Références

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Auteurs

Daniel J Sheward (DJ)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.

Changil Kim (C)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.

Roy A Ehling (RA)

Department of Biosystems Science and Engineering, ETH Zürich, Zürich, Switzerland.

Alec Pankow (A)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.

Xaquin Castro Dopico (X)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.

Robert Dyrdak (R)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden.

Darren P Martin (DP)

Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.

Sai T Reddy (ST)

Department of Biosystems Science and Engineering, ETH Zürich, Zürich, Switzerland.

Joakim Dillner (J)

Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.

Gunilla B Karlsson Hedestam (GB)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.

Jan Albert (J)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden.

Ben Murrell (B)

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. Electronic address: benjamin.murrell@ki.se.

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Classifications MeSH