Plaque-neutralizing antibody to BA.2.12.1, BA.4 and BA.5 in individuals with three doses of BioNTech or CoronaVac vaccines, natural infection and breakthrough infection.


Journal

Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology
ISSN: 1873-5967
Titre abrégé: J Clin Virol
Pays: Netherlands
ID NLM: 9815671

Informations de publication

Date de publication:
11 2022
Historique:
received: 15 07 2022
revised: 22 08 2022
accepted: 26 08 2022
pubmed: 10 9 2022
medline: 12 10 2022
entrez: 9 9 2022
Statut: ppublish

Résumé

BA.2.12.1, BA.4 and BA.5 subvariants of SARS-CoV-2 variant-of-concern (VOC) Omicron (B.1.1.529) are spreading globally. They demonstrate higher transmissibility and immune escape. Determine BA.2.12.1, BA.4 and BA.5 virus plaque reduction neutralization test (PRNT) antibody titres in individuals recently vaccinated with BNT162b2 (n = 20) or CoronaVac (n = 20) vaccines or those convalescent from ancestral wild- type (WT) SARS-CoV-2 (n = 20) or BA.2 infections with (n = 17) or without (n = 7) prior vaccination. Relative to neutralization of the WT virus, those vaccinated with BNT162b2 had 4.8, 3.4, 4.6, 11.3 and 15.5-fold reductions of geometric mean antibody titres (GMT) to BA.1, BA.2, BA.2.12.1, BA.4 and BA.5 viruses, respectively. Similarly, those vaccinated with CoronaVac had 8.0, 7.0, 11.8, 12.0 and 12.0 fold GMT reductions and those with two doses of CoronaVac boosted by BNT162b2 had 6.1, 6.7, 6,3, 13.0 and 21.2 fold GMT reductions to these viruses, respectively. Vaccinated individuals with BA.2 breakthrough infections had higher GMT antibody levels vs. BA.4 (36.9) and BA.5 (36.9) than unvaccinated individuals with BA.2 infections (BA.4 GMT 8.2; BA.5 GMT 11.0). BA.4 and BA.5 subvariants were less susceptible to BNT162b2 or CoronaVac vaccine elicited antibody neutralization than subvariants BA.1, BA.2 and BA.2.12.1. Nevertheless, three doses BNT162b2 or booster of BNT162b2 following two doses of CoronaVac elicited detectable BA.4 and BA.5 neutralizing antibody responses while those vaccinated with three doses of CoronaVac largely fail to do so. BA.2 infections in vaccinated individuals led to higher levels of BA.4 or BA.5 neutralizing antibody compared to those who were vaccine-naive.

Sections du résumé

BACKGROUND
BA.2.12.1, BA.4 and BA.5 subvariants of SARS-CoV-2 variant-of-concern (VOC) Omicron (B.1.1.529) are spreading globally. They demonstrate higher transmissibility and immune escape.
OBJECTIVES
Determine BA.2.12.1, BA.4 and BA.5 virus plaque reduction neutralization test (PRNT) antibody titres in individuals recently vaccinated with BNT162b2 (n = 20) or CoronaVac (n = 20) vaccines or those convalescent from ancestral wild- type (WT) SARS-CoV-2 (n = 20) or BA.2 infections with (n = 17) or without (n = 7) prior vaccination.
RESULTS
Relative to neutralization of the WT virus, those vaccinated with BNT162b2 had 4.8, 3.4, 4.6, 11.3 and 15.5-fold reductions of geometric mean antibody titres (GMT) to BA.1, BA.2, BA.2.12.1, BA.4 and BA.5 viruses, respectively. Similarly, those vaccinated with CoronaVac had 8.0, 7.0, 11.8, 12.0 and 12.0 fold GMT reductions and those with two doses of CoronaVac boosted by BNT162b2 had 6.1, 6.7, 6,3, 13.0 and 21.2 fold GMT reductions to these viruses, respectively. Vaccinated individuals with BA.2 breakthrough infections had higher GMT antibody levels vs. BA.4 (36.9) and BA.5 (36.9) than unvaccinated individuals with BA.2 infections (BA.4 GMT 8.2; BA.5 GMT 11.0).
CONCLUSIONS
BA.4 and BA.5 subvariants were less susceptible to BNT162b2 or CoronaVac vaccine elicited antibody neutralization than subvariants BA.1, BA.2 and BA.2.12.1. Nevertheless, three doses BNT162b2 or booster of BNT162b2 following two doses of CoronaVac elicited detectable BA.4 and BA.5 neutralizing antibody responses while those vaccinated with three doses of CoronaVac largely fail to do so. BA.2 infections in vaccinated individuals led to higher levels of BA.4 or BA.5 neutralizing antibody compared to those who were vaccine-naive.

Identifiants

pubmed: 36081282
pii: S1386-6532(22)00205-0
doi: 10.1016/j.jcv.2022.105273
pmc: PMC9428331
pii:
doi:

Substances chimiques

Antibodies, Neutralizing 0
Antibodies, Viral 0
COVID-19 Vaccines 0
Viral Vaccines 0
BNT162 Vaccine N38TVC63NU

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

105273

Subventions

Organisme : NIAID NIH HHS
ID : U01 AI151810
Pays : United States

Informations de copyright

Copyright © 2022. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing Interest None of the authors had competing financial or non-financial interests.

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Auteurs

Samuel Sm Cheng (SS)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Chris Kp Mok (CK)

The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

John Kc Li (JK)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Susanna S Ng (SS)

Department of Medicine & Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Bosco Hs Lam (BH)

Department of Pathology, North Lantau Hospital, Hong Kong SAR, China.

Trushar Jeevan (T)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Ahmed Kandeil (A)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Andrew Pekosz (A)

W. Harry Feinstone Department of Molecular Microbiology and Immunology, The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA.

Karl Ck Chan (KC)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Leo Ch Tsang (LC)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Fanny W Ko (FW)

Department of Medicine & Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Chunke Chen (C)

The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong SAR, China; Li Ka Shing Institute of Health Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Karen Yiu (K)

Department of Medicine & Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Leo Lh Luk (LL)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

Ken Kp Chan (KK)

Department of Medicine & Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Richard J Webby (RJ)

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, Tennessee, USA.

Leo Lm Poon (LL)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China.

David Sc Hui (DS)

Department of Medicine & Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China; Stanley Ho Centre for Emerging Infectious Diseases, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong SAR, China.

Malik Peiris (M)

School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong SAR, China; Centre for Immunology and Infection, Hong Kong Science Park, Shatin, Hong Kong SAR, China. Electronic address: malik@hku.hk.

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