Evidence map›Paper›PMID 36090991›Full record

ArticleFrontiers in immunology2022

Targeted escape of SARS-CoV-2

Clara Luzia Magnus, Andreas Hiergeist, Philipp Schuster, Anette Rohrhofer, Jan Medenbach, André Gessner, David Peterhoff, Barbara Schmidt

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 27 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

8 authors at 3 institutions in 1 country.

Clara Luzia MagnusInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Andreas HiergeistInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Philipp SchusterInstitute of Medical Microbiology and Hygiene, University of Regensburg, Regensburg, Germany.
Anette RohrhoferInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Jan MedenbachBiochemistry I, Faculty of Biology and Pre-Clinical Medicine, University of Regensburg, Regensburg, Germany.
André GessnerInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
David PeterhoffInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
Barbara SchmidtInstitute of Clinical Microbiology and Hygiene, University Hospital Regensburg, Regensburg, Germany.
University Hospital Regensburg · DEUniversity of Regensburg · DEInstitute of Medical Microbiology and Hygiene · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Class 1 and 2 monoclonal antibodies inhibit SARS-CoV-2 entry by blocking the interaction of the viral receptor-binding domain with angiotensin-converting enzyme 2 (ACE2), while class 3 antibodies target a highly conserved epitope outside the ACE2 binding site. We aimed to investigate the plasticity of the spike protein by propagating wild-type SARS-CoV-2 in the presence of class 3 antibody S309. After 12 weeks, we obtained a viral strain that was completely resistant to inhibition by S309, due to successively evolving amino acid exchanges R346S and P337L located in the paratope of S309. The antibody lost affinity to receptor-binding domains carrying P337L or both amino acid exchanges, while ACE2 binding was not affected. The resistant strain replicated efficiently in human CaCo-2 cells and was more susceptible to inhibition of fusion than the original strain. Overall, SARS-CoV-2 escaped inhibition by class 3 antibody S309 through a slow, but targeted evolution enabling immune escape and altering cell entry. This immune-driven enhancement of infectivity and pathogenicity could play an important role in the future evolution of SARS-CoV-2, which is under increasing immunological pressure from vaccination and previous infections.

Indexed as

Angiotensin-Converting Enzyme 2COVID-19Amino AcidsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingCaco-2 CellsHumansPeptidyl-Dipeptidase ASARS-CoV-2Spike Glycoprotein, CoronavirusAmino AcidsAngiotensin-Converting Enzyme 2Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingPeptidyl-Dipeptidase AsotrovimabSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2endocytosisentryfusionimmune escapemonoclonal antibodyreceptor-binding domainSARS-CoV-2sotrovimab

Identifiers

PMID36090991
PMCPMC9449809
OpenAlexW4293113296

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.