Evidence map›Paper›PMID 41134631›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2025

Glycan recognition by collectin-11 drives SARS-CoV-2 infectivity and membrane injury of respiratory epithelial cells.

Anastasia Polycarpou, Tara Wagner-Gamble, Roseanna Greenlaw, Lauren O'Neill, Varsha Kanabar, Alanoud Alrehaili, Yusun Jeon, Jonathan Baker, Mona Bafadhel, Hataf Khan and 9 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Glycan recognition by collectin-11 drives SARS-CoV-2 infectivity and membrane injury of respiratory epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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.

Anastasia Polycarpou *Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.
Tara Wagner-Gamble *Department of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Roseanna Greenlaw *Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.
Lauren O'Neill *Department of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Varsha KanabarDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Alanoud AlrehailiDepartment of Respiratory Sciences, University of Leicester, Leicester LE1 9HN, United Kingdom.
Yusun JeonPeter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.ORCID 0000-0001-5031-8656
Jonathan BakerKing's Centre for Lung Health, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Mona BafadhelKing's Centre for Lung Health, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Hataf KhanDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Michael H MalimDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.ORCID 0000-0002-7699-2064
Marco RomanoPeter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.
Conrad A FarrarPeter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.ORCID 0000-0001-9627-9293
Dorota SmolarekPeter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.
Rocio Martinez-NunezDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Katie J DooresDepartment of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.
Russell WallisDepartment of Respiratory Sciences, University of Leicester, Leicester LE1 9HN, United Kingdom.
Linda S Klavinskis *Department of Infectious Diseases, School of Immunology and Microbial Sciences, King's College London, London SE1 9RT, United Kingdom.ORCID 0000-0001-5828-6978
Steven H Sacks *Peter Gorer Department of Immunobiology, School of Immunology and Microbial Sciences, King's College, London SE1 9RT, United Kingdom.ORCID 0000-0001-6361-9095

Funding

British Society for Antimicrobial Chemotherapy (BSAC) BSAC-COVID-57Wellcome TrustWellcome Trust (WT) 222433/Z/21/Z
6 · The paper itself

Abstract

SARS-CoV-2 respiratory-tract infection affects both vaccinated and unvaccinated persons suggesting factors besides adaptive immunity are operative. We investigated the role of collectin-11 (CL-11), an epithelial-secreted carbohydrate-binding lectin that drives innate immunity and eliminates pathogens by complement activation. SARS-CoV-2, despite binding CL-11 to activate complement, was resistant to lysis. Remarkably, opsonization by CL-11 enhanced virus production by infected respiratory epithelial cells independently of complement. Furthermore, infected cells expressing SARS-CoV-2 spike protein displayed enhanced vulnerability to CL-11 binding and membrane attack by complement. The mechanism of enhanced infectivity was ablated in the presence of L-fucose, which occupied the extended carbohydrate-binding cleft of CL-11 in a crystallographic analysis of complexes between L-fucose and CL-11. Our study suggests pathogenicity of SARS-CoV-2 is related to complement-resistance together with enhanced infectivity and injury of respiratory epithelial cells mediated by locally released CL-11.

Indexed as

CollectinsCOVID-19Epithelial CellsPolysaccharidesRespiratory MucosaSARS-CoV-2Cell MembraneComplement ActivationComplement System ProteinsHumansImmunity, InnateProtein BindingSpike Glycoprotein, CoronavirusColec11 protein, humanCollectinsComplement System ProteinsPolysaccharidesSpike Glycoprotein, Coronavirusspike protein, SARS-CoV-2collectin-11complement proteinsglycansSARS-CoV-2

Identifiers

PMID41134631
PMCPMC12582335

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.