Evidence map›Paper›PMID 35305699›Full record

ArticleThe Lancet. Infectious diseases2022

Neutralisation sensitivity of the SARS-CoV-2 omicron (B.1.1.529) variant: a cross-sectional study.

Daniel J Sheward, Changil Kim, Roy A Ehling, Alec Pankow, Xaquin Castro Dopico, Robert Dyrdak, Darren P Martin, Sai T Reddy, Joakim Dillner, Gunilla B Karlsson Hedestam and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Lancet. Infectious diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
9.3field-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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 93 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

12 authors at 4 institutions in 3 countries.

Daniel J ShewardDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Changil KimDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Roy A EhlingDepartment of Biosystems Science and Engineering, ETH Zürich, Zürich, Switzerland.
Alec PankowDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Xaquin Castro DopicoDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Robert DyrdakDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden.
Darren P MartinInstitute of Infectious Diseases and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Sai T ReddyDepartment of Biosystems Science and Engineering, ETH Zürich, Zürich, Switzerland.
Joakim DillnerDepartment of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
Gunilla B Karlsson HedestamDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
Jan AlbertDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Microbiology, Karolinska University Hospital, Stockholm, Sweden.
Ben MurrellDepartment of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. Electronic address: benjamin.murrell@ki.se.
Karolinska Institutet · SEETH Zurich · CHKarolinska University Hospital · SEUniversity of Cape Town · ZA

Funding

Medical Research Council MR/W005611/1
6 · The paper itself

Abstract

backgroundThe SARS-CoV-2 omicron (B.1.1.529) variant, which was first identified in November, 2021, spread rapidly in many countries, with a spike protein highly diverged from previously known variants, and raised concerns that this variant might evade neutralising antibody responses. We therefore aimed to characterise the sensitivity of the omicron variant to neutralisation.

methodsFor this cross-sectional study, we cloned the sequence encoding the omicron spike protein from a diagnostic sample to establish an omicron pseudotyped virus neutralisation assay. We quantified the neutralising antibody ID

findingsNeutralising antibody responses in reference sample pools sampled shortly after infection or vaccination were substantially less potent against the omicron variant than against wild-type SARS-CoV-2 (seven-fold to 42-fold reduction in ID

interpretationThese data highlight the extensive, but incomplete, evasion of neutralising antibody responses by the omicron variant, and suggest that boosting with licensed vaccines might be sufficient to raise neutralising antibody titres to protective levels.

fundingEuropean Union Horizon 2020 research and innovation programme, European and Developing Countries Clinical Trials Partnership, SciLifeLab, and the Erling-Persson Foundation.

Indexed as

COVID-19SARS-CoV-2Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingAntibodies, ViralCOVID-19 VaccinesCross-Sectional StudiesHumansSpike Glycoprotein, CoronavirusAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntibodies, NeutralizingAntibodies, ViralbamlanivimabcasirivimabCOVID-19 VaccinesetesevimabimdevimabsotrovimabSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2

Identifiers

PMID35305699
PMCPMC8930016
OpenAlexW4221067052

What OpenQuestion holds

Textmetadata
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.