Evidence map›Paper›PMID 37699890›Full record

ArticleNature communications2023

Previous immunity shapes immune responses to SARS-CoV-2 booster vaccination and Omicron breakthrough infection risk.

Laura Pérez-Alós, Cecilie Bo Hansen, Jose Juan Almagro Armenteros, Johannes Roth Madsen, Line Dam Heftdal, Rasmus Bo Hasselbalch, Mia Marie Pries-Heje, Rafael Bayarri-Olmos, Ida Jarlhelt, Sebastian Rask Hamm and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
9.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 4 institutions in 2 countries.

Laura Pérez-AlósLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. laura.perez.alos@regionh.dk.ORCID http://orcid.org/0000-0002-0368-4976
Cecilie Bo HansenLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-7709-4522
Jose Juan Almagro ArmenterosDepartment of Genetics, Stanford University School of Medicine, Stanford, 94305, CA, USA.
Johannes Roth MadsenLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Line Dam HeftdalViro-immunology Research Unit, Department of Infectious Diseases, Section 8632, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-6946-7341
Rasmus Bo HasselbalchDepartment of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Copenhagen, Denmark.
Mia Marie Pries-HejeThe Heart Center, Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Rafael Bayarri-OlmosLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-3202-9679
Ida JarlheltLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-3576-5025
Sebastian Rask HammViro-immunology Research Unit, Department of Infectious Diseases, Section 8632, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Dina Leth MøllerViro-immunology Research Unit, Department of Infectious Diseases, Section 8632, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0002-3909-0643
Erik SørensenDepartment of Clinical Immunology, Section 2034, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Sisse Rye OstrowskiDepartment of Clinical Immunology, Section 2034, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.ORCID http://orcid.org/0000-0001-5288-3851
Ruth Frikke-SchmidtDepartment of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.ORCID http://orcid.org/0000-0003-4084-5027
Linda Maria HilstedDepartment of Clinical Biochemistry, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Henning BundgaardThe Heart Center, Department of Cardiology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Susanne Dam NielsenViro-immunology Research Unit, Department of Infectious Diseases, Section 8632, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark.
Kasper Karmark IversenDepartment of Cardiology, Copenhagen University Hospital Herlev and Gentofte, Copenhagen, Denmark.
Peter GarredLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark. peter.garred@regionh.dk.ORCID http://orcid.org/0000-0002-2876-8586
Copenhagen University Hospital · DKUniversity of Copenhagen · DKGentofte Hospital · DKStanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heterogeneity of the SARS-CoV-2 immune responses has become considerably more complex over time and diverse immune imprinting is observed in vaccinated individuals. Despite vaccination, following the emergence of the Omicron variant, some individuals appear more susceptible to primary infections and reinfections than others, underscoring the need to elucidate how immune responses are influenced by previous infections and vaccination. IgG, IgA, neutralizing antibodies and T-cell immune responses in 1,325 individuals (955 of which were infection-naive) were investigated before and after three doses of the BNT162b2 vaccine, examining their relation to breakthrough infections and immune imprinting in the context of Omicron. Our study shows that both humoral and cellular responses following vaccination were generally higher after SARS-CoV-2 infection compared to infection-naive. Notably, viral exposure before vaccination was crucial to achieving a robust IgA response. Individuals with lower IgG, IgA, and neutralizing antibody responses postvaccination had a significantly higher risk of reinfection and future Omicron infections. This was not observed for T-cell responses. A primary infection before Omicron and subsequent reinfection with Omicron dampened the humoral and cellular responses compared to a primary Omicron infection, consistent with immune imprinting. These results underscore the significant impact of hybrid immunity for immune responses in general, particularly for IgA responses even after revaccination, and the importance of robust humoral responses in preventing future infections.

Indexed as

Breakthrough InfectionsCOVID-19Antibodies, NeutralizingBNT162 VaccineHumansImmunityImmunoglobulin AImmunoglobulin GReinfectionSARS-CoV-2VaccinationAntibodies, NeutralizingBNT162 VaccineImmunoglobulin AImmunoglobulin G

Identifiers

PMID37699890
PMCPMC10497567
OpenAlexW4386691525

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.