Evidence map›Paper›PMID 33564766›Full record

ArticlebioRxiv : the preprint server for biology2021

Impact of the B.1.1.7 variant on neutralizing monoclonal antibodies recognizing diverse epitopes on SARS-CoV-2 Spike.

Carl Graham, Jeffrey Seow, Isabella Huettner, Hataf Khan, Neophytos Kouphou, Sam Acors, Helena Winstone, Suzanne Pickering, Rui Pedro Galao, Maria Jose Lista and 17 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed, 32 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

27 authors at 4 institutions in 1 country.

Carl GrahamDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Jeffrey SeowDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Isabella HuettnerDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Hataf KhanDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Neophytos KouphouDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Sam AcorsDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Helena WinstoneDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Suzanne PickeringDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Rui Pedro GalaoDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Maria Jose ListaDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Jose M Jimenez-GuardenoDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Adam G LaingPeter Gorer Department of Immunobiology, School of Immunology & Microbial Sciences, King's College London, London, UK.
Yin WuPeter Gorer Department of Immunobiology, School of Immunology & Microbial Sciences, King's College London, London, UK.
Magdalene JosephPeter Gorer Department of Immunobiology, School of Immunology & Microbial Sciences, King's College London, London, UK.
Luke MuirDivision of Infection and Immunity, University College London, London, UK.
Weng M NgDivision of Structural Biology, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Helen M E DuyvesteynDivision of Structural Biology, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Yuguang ZhaoDivision of Structural Biology, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Thomas A BowdenDivision of Structural Biology, Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK.
Manu Shankar-HariDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Annachiara RosaThe Francis Crick Institute, UK.
Peter CherepanovThe Francis Crick Institute, UK.
Laura E McCoyDivision of Infection and Immunity, University College London, London, UK.
Adrian C HaydayDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Stuart J D NeilDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Michael H MalimDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
Katie J DooresDepartment of Infectious Diseases, School of Immunology & Microbial Sciences, King's College London, London, UK.
King's College London · GBCentre for Human Genetics · GBThe Francis Crick Institute · GBUniversity College London · GB

Funding

X-ray Crystallographic Fragment Screening CoreU54AI150472 · NIAID · SEATTLE CHILDREN'S HOSPITAL · PI LYUMKIS, DMITRY · 2019 to 2021
$15.7M
Medical Research Council MR/R008698/1Medical Research Council MR/S007555/1NIAID NIH HHS U54 AI150472Wellcome Trust FC001061
6 · The paper itself

Abstract

The interaction of the SARS-CoV-2 Spike receptor binding domain (RBD) with the ACE2 receptor on host cells is essential for viral entry. RBD is the dominant target for neutralizing antibodies and several neutralizing epitopes on RBD have been molecularly characterized. Analysis of circulating SARS-CoV-2 variants has revealed mutations arising in the RBD, the N-terminal domain (NTD) and S2 subunits of Spike. To fully understand how these mutations affect the antigenicity of Spike, we have isolated and characterized neutralizing antibodies targeting epitopes beyond the already identified RBD epitopes. Using recombinant Spike as a sorting bait, we isolated >100 Spike-reactive monoclonal antibodies from SARS-CoV-2 infected individuals. ≈45% showed neutralizing activity of which ≈20% were NTD-specific. None of the S2-specific antibodies showed neutralizing activity. Competition ELISA revealed that NTD-specific mAbs formed two distinct groups: the first group was highly potent against infectious virus, whereas the second was less potent and displayed glycan-dependant neutralization activity. Importantly, mutations present in B.1.1.7 Spike frequently conferred resistance to neutralization by the NTD-specific neutralizing antibodies. This work demonstrates that neutralizing antibodies targeting subdominant epitopes need to be considered when investigating antigenic drift in emerging variants.

Identifiers

PMID33564766
PMCPMC7872354
OpenAlexW3127921995

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.