Limited neutralisation of the SARS-CoV-2 Omicron subvariants BA.1 and BA.2 by convalescent and vaccine serum and monoclonal antibodies.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Aug 2022
Historique:
received: 05 03 2022
revised: 23 06 2022
accepted: 28 06 2022
pubmed: 15 7 2022
medline: 17 8 2022
entrez: 14 7 2022
Statut: ppublish

Résumé

In recent months, Omicron variants of SARS-CoV-2 have become dominant in many regions of the world, and case numbers with Omicron subvariants BA.1 and BA.2 continue to increase. Due to numerous mutations in the spike protein, the efficacy of currently available vaccines, which are based on Wuhan-Hu 1 isolate of SARS-CoV-2, is reduced, leading to breakthrough infections. Efficacy of monoclonal antibody therapy is also likely impaired. In our in vitro study using A549-AT cells constitutively expressing ACE2 and TMPRSS2, we determined and compared the neutralizing capacity of vaccine-elicited sera, convalescent sera and monoclonal antibodies against authentic SARS-CoV-2 Omicron BA.1 and BA.2 compared with Delta. Almost no neutralisation of Omicron BA.1 and BA.2 was observed using sera from individuals vaccinated with two doses 6 months earlier, regardless of the type of vaccine taken. Shortly after the booster dose, most sera from triple BNT162b2-vaccinated individuals were able to neutralise both Omicron variants. In line with waning antibody levels three months after the booster, only weak residual neutralisation was observed for BA.1 (26%, n = 34, 0 median NT Both SARS-CoV-2 Omicron subvariants BA.1 and BA.2 escape antibody-mediated neutralisation elicited by vaccination, previous infection with SARS-CoV-2, and monoclonal antibodies. Waning immunity renders the majority of tested sera obtained three months after booster vaccination negative in BA.1 and BA.2 neutralisation. Omicron subvariant specific resistance to the monoclonal antibodies casirivimab/imdevimab and sotrovimab emphasizes the importance of genotype-surveillance and guided application. This study was supported in part by the Goethe-Corona-Fund of the Goethe University Frankfurt (M.W.) and the Federal Ministry of Education and Research (COVIDready; grant 02WRS1621C (M.W.).

Sections du résumé

BACKGROUND BACKGROUND
In recent months, Omicron variants of SARS-CoV-2 have become dominant in many regions of the world, and case numbers with Omicron subvariants BA.1 and BA.2 continue to increase. Due to numerous mutations in the spike protein, the efficacy of currently available vaccines, which are based on Wuhan-Hu 1 isolate of SARS-CoV-2, is reduced, leading to breakthrough infections. Efficacy of monoclonal antibody therapy is also likely impaired.
METHODS METHODS
In our in vitro study using A549-AT cells constitutively expressing ACE2 and TMPRSS2, we determined and compared the neutralizing capacity of vaccine-elicited sera, convalescent sera and monoclonal antibodies against authentic SARS-CoV-2 Omicron BA.1 and BA.2 compared with Delta.
FINDINGS RESULTS
Almost no neutralisation of Omicron BA.1 and BA.2 was observed using sera from individuals vaccinated with two doses 6 months earlier, regardless of the type of vaccine taken. Shortly after the booster dose, most sera from triple BNT162b2-vaccinated individuals were able to neutralise both Omicron variants. In line with waning antibody levels three months after the booster, only weak residual neutralisation was observed for BA.1 (26%, n = 34, 0 median NT
INTERPRETATION CONCLUSIONS
Both SARS-CoV-2 Omicron subvariants BA.1 and BA.2 escape antibody-mediated neutralisation elicited by vaccination, previous infection with SARS-CoV-2, and monoclonal antibodies. Waning immunity renders the majority of tested sera obtained three months after booster vaccination negative in BA.1 and BA.2 neutralisation. Omicron subvariant specific resistance to the monoclonal antibodies casirivimab/imdevimab and sotrovimab emphasizes the importance of genotype-surveillance and guided application.
FUNDING BACKGROUND
This study was supported in part by the Goethe-Corona-Fund of the Goethe University Frankfurt (M.W.) and the Federal Ministry of Education and Research (COVIDready; grant 02WRS1621C (M.W.).

Identifiants

pubmed: 35834885
pii: S2352-3964(22)00339-5
doi: 10.1016/j.ebiom.2022.104158
pmc: PMC9271884
pii:
doi:

Substances chimiques

Antibodies, Monoclonal 0
Antibodies, Monoclonal, Humanized 0
Antibodies, Neutralizing 0
Antibodies, Viral 0
Viral Vaccines 0
sotrovimab 1MTK0BPN8V
imdevimab 2Z3DQD2JHM
casirivimab J0FI6WE1QN
BNT162 Vaccine N38TVC63NU

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

104158

Informations de copyright

Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests S.H. has received research support from Roche Diagnostics and a speaker's fee from Sanofi Genzyme. T.W. has received speaker and consultancy fees from Gilead Sciences, Merck Sharp & Dohme, and Janssen Pharmaceuticals. N.K. received speaker fees from Abbott. S.C. was a member of a clinical advisory board for Biontech. All other authors declare no conflicts of interest, financial or otherwise.

Auteurs

Alexander Wilhelm (A)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Marek Widera (M)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany. Electronic address: marek.widera@kgu.de.

Katharina Grikscheit (K)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Tuna Toptan (T)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Barbara Schenk (B)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Christiane Pallas (C)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Melinda Metzler (M)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Niko Kohmer (N)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Sebastian Hoehl (S)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Rolf Marschalek (R)

Institute of Pharmaceutical Biology, Goethe University, Frankfurt am Main, Germany.

Eva Herrmann (E)

Institute of Biostatistics and Mathematical Modelling, Goethe University Frankfurt, 60596 Frankfurt, Germany.

Fabian A Helfritz (FA)

Bürgerhospital Frankfurt, Nibelungenallee 37-41, 60318 Frankfurt am Main, Germany.

Timo Wolf (T)

Department of Internal Medicine, Infectious Diseases, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany.

Udo Goetsch (U)

Health Protection Authority of the City of Frankfurt am Main, 60313 Frankfurt am Main, Germany.

Sandra Ciesek (S)

Institute for Medical Virology, University Hospital Frankfurt, Goethe University Frankfurt, 60596 Frankfurt am Main, Germany; German Centre for Infection Research (DZIF), partner site Frankfurt, Germany; Fraunhofer Institute for Molecular Biology and Applied Ecology, Branch Translational Medicine and Pharmacology, 60596 Frankfurt am Main, Germany. Electronic address: sandra.ciesek@kgu.de.

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Classifications MeSH