Evidence map›Paper›PMID 38953380›Full record

ArticleJournal of virology2024

SARS-CoV-2 BA.4/5 infection triggers more cross-reactive FcγRIIIa signaling and neutralization than BA.1, in the context of hybrid immunity.

Simone I Richardson, Nonkululeko Mzindle, Thopisang Motlou, Nelia P Manamela, Mieke A van der Mescht, Bronwen E Lambson, Josie Everatt, Daniel Gyamfi Amoako, Sashkia Balla, Anne von Gottberg and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

21 authors.

Simone I RichardsonSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.ORCID 0000-0001-7678-2609
Nonkululeko MzindleSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Thopisang MotlouSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Nelia P ManamelaSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Mieke A van der MeschtDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa.
Bronwen E LambsonSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Josie EverattSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Daniel Gyamfi AmoakoSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Sashkia BallaSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Anne von GottbergSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Nicole WolterSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Zelda de BeerTshwane District Hospital, Pretoria, South Africa.
Talita Roma de VilliersTshwane District Hospital, Pretoria, South Africa.
Annie BodensteinTshwane District Hospital, Pretoria, South Africa.
Gretha van den BergTshwane District Hospital, Pretoria, South Africa.
Fareed AbdullahDivision for Infectious Diseases, Department of Internal Medicine, Steve Biko Academic Hospital and University of Pretoria, Pretoria, South Africa.
Theresa M RossouwDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria, South Africa.
Michael T BoswellDivision for Infectious Diseases, Department of Internal Medicine, Steve Biko Academic Hospital and University of Pretoria, Pretoria, South Africa.
Veronica UeckermannDivision for Infectious Diseases, Department of Internal Medicine, Steve Biko Academic Hospital and University of Pretoria, Pretoria, South Africa.
Jinal N BhimanSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.
Penny L MooreSAMRC Antibody Immunity Research Unit, School of Pathology, University of the Witwatersrand, Johannesburg, South Africa.ORCID 0000-0001-8719-4028

Funding

Gates Foundation INV-018978Gates Foundation INV-030570South African Medical Research Council (SAMRC) 96847
6 · The paper itself

Abstract

SARS-CoV-2 variants of concern (VOCs) differentially trigger neutralizing and antibody-dependent cellular cytotoxic (ADCC) antibodies with variable cross-reactivity. Omicron BA.4/5 was approved for inclusion in bivalent vaccination boosters, and therefore the antigenic profile of antibodies elicited by this variant is critical to understand. Here, we investigate the ability of BA.4/5-elicited antibodies following the first documented (primary) infection ( IMPORTANCE: The continued evolution of SARS-CoV-2 has resulted in a number of variants of concern. Of these, the Omicron sublineage is the most immune evasive. Within Omicron, the BA.4/5 sublineage drove the fifth wave of infection in South Africa prior to becoming the dominant variant globally. As a result this spike sequence was approved as part of a bivalent vaccine booster, and rolled out worldwide. We aimed to understand the cross-reactivity of neutralizing and Fc mediated cytotoxic functions elicited by BA.4/5 infection following infection or breakthrough infection. We find that, in contrast to BA.1 which triggered fairly strain-specific antibodies, BA.4/5 triggered antibodies that are highly cross-reactive for neutralization and antibody-dependent cellular cytotoxicity potential. Despite this cross-reactivity, these antibodies are compromised against highly resistant variants such as XBB.1.5 and BQ.1. This suggests that next-generation vaccines will require XBB sublineage immunogens in order to protect against these evasive variants.

Indexed as

Antibodies, NeutralizingAntibodies, ViralAntibody-Dependent Cell CytotoxicityCOVID-19Cross ReactionsReceptors, IgGSARS-CoV-2Signal TransductionCOVID-19 VaccinesHumansNeutralization TestsSpike Glycoprotein, CoronavirusAntibodies, NeutralizingAntibodies, ViralCOVID-19 VaccinesFCGR3A protein, humanReceptors, IgGSpike Glycoprotein, Coronavirusantibody-dependent cellular cytotoxicityBA.1BA.5breakthrough infectionneutralizationOmicron BA.4SARS-CoV-2variant of concernXBB sublineage

Identifiers

PMID38953380
PMCPMC11265454

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Registered trials

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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.