Evidence map›Paper›PMID 37051252›Full record

ArticleFrontiers in immunology2023

Complement lectin pathway activation is associated with COVID-19 disease severity, independent of

Lisa Hurler, Ágnes Szilágyi, Federica Mescia, Laura Bergamaschi, Blanka Mező, György Sinkovits, Marienn Réti, Veronika Müller, Zsolt Iványi, János Gál and 19 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

18 citing papers in PubMed, 24 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

29 authors at 4 institutions in 4 countries.

Lisa HurlerDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Ágnes SzilágyiDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Federica MesciaCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge, United Kingdom.
Laura BergamaschiCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge, United Kingdom.
Blanka MezőDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
György SinkovitsDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Marienn RétiDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Veronika MüllerDepartment of Pulmonology, Semmelweis University, Budapest, Hungary.
Zsolt IványiDepartment of Anaesthesiology and Intensive Therapy, Semmelweis University, Budapest, Hungary.
János GálDepartment of Anaesthesiology and Intensive Therapy, Semmelweis University, Budapest, Hungary.
László GopcsaDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Péter ReményiDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Beáta SzathmáryDepartment of Infectology, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Botond LakatosDepartment of Infectology, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
János SzlávikDepartment of Infectology, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Ilona BobekDepartment of Anaesthesiology and Intensive Therapy, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Zita Z ProhászkaDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Zsolt FörhéczDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Dorottya CsukaDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Erika KajdácsiDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
László CervenakDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Petra KiszelResearch Group for Immunology and Haematology, Semmelweis University - Eötvös Loránd Research Network (Office for Supported Research Groups), Budapest, Hungary.
Tamás MassziDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
István Vályi-NagyDepartment of Haematology and Stem Cell Transplantation, Central Hospital of Southern Pest - Institute of Haematology and Infectious Diseases, Budapest, Hungary.
Reinhard WürznerInstitute of Hygiene and Medical Microbiology, Medical University of Innsbruck, Innsbruck, Austria.
Cambridge Institute of Therapeutic Immunology and Infectious Disease-National Institute of Health Research (CITIID-NIHR) COVID BioResource Collaboration
Paul A LyonsCambridge Institute of Therapeutic Immunology and Infectious Disease, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge, United Kingdom.
Erik J M ToonenResearch and Development Department, Hycult Biotech, Uden, Netherlands.
Zoltán ProhászkaDepartment of Internal Medicine and Haematology, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUNational Center for Epidemiology · HUUniversity of Cambridge · GBInnsbruck Medical University · AT

Funding

Department of Health
6 · The paper itself

Abstract

Introduction: While complement is a contributor to disease severity in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections, all three complement pathways might be activated by the virus. Lectin pathway activation occurs through different pattern recognition molecules, including mannan binding lectin (MBL), a protein shown to interact with SARS-CoV-2 proteins. However, the exact role of lectin pathway activation and its key pattern recognition molecule MBL in COVID-19 is still not fully understood. Methods: We therefore investigated activation of the lectin pathway in two independent cohorts of SARS-CoV-2 infected patients, while also analysing MBL protein levels and potential effects of the six major single nucleotide polymorphisms (SNPs) found in the MBL2 gene on COVID-19 severity and outcome. Results: We show that the lectin pathway is activated in acute COVID-19, indicated by the correlation between complement activation product levels of the MASP-1/C1-INH complex (p=0.0011) and C4d (p<0.0001) and COVID-19 severity. Despite this, genetic variations in MBL2 are not associated with susceptibility to SARS-CoV-2 infection or disease outcomes such as mortality and the development of Long COVID. Conclusion: In conclusion, activation of the MBL-LP only plays a minor role in COVID-19 pathogenesis, since no clinically meaningful, consistent associations with disease outcomes were noted.

Indexed as

COVID-19Mannose-Binding LectinGenotypeHumansLectinsPatient AcuityPost-Acute COVID-19 SyndromeSARS-CoV-2LectinsMannose-Binding LectinMBL2 protein, humanCOVID-19lectin pathway activationlectin pathway of complementmannose binding lectin (MBL)MBL2 genotypessevere acute respiratory coronavirus 2 (SARS-CoV-2)

Identifiers

PMID37051252
PMCPMC10084477
OpenAlexW4361224213

What OpenQuestion holds

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LicenceCC BY
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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.