Evidence map›Paper›PMID 37620330›Full record

Articlenpj aging2023

Severe COVID-19 patients exhibit elevated levels of autoantibodies targeting cardiolipin and platelet glycoprotein with age: a systems biology approach.

Dennyson Leandro M Fonseca, Igor Salerno Filgueiras, Alexandre H C Marques, Elroy Vojdani, Gilad Halpert, Yuri Ostrinski, Gabriela Crispim Baiocchi, Desirée Rodrigues Plaça, Paula P Freire, Shahab Zaki Pour and 20 more

Open access · hybridAbstract read
In one paragraph

Article in npj aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 38 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

30 authors at 14 institutions in 9 countries.

Dennyson Leandro M Fonseca *Interunit Postgraduate Program on Bioinformatics, Institute of Mathematics and Statistics (IME), University of Sao Paulo (USP), Sao Paulo, SP, Brazil. dennyson@usp.br.ORCID http://orcid.org/0000-0003-2567-5808
Igor Salerno Filgueiras *Department of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.ORCID http://orcid.org/0000-0002-3493-4464
Alexandre H C MarquesDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.ORCID http://orcid.org/0000-0002-0515-6990
Elroy VojdaniRegenera Medical 11860 Wilshire Blvd., Ste. 301, Los Angeles, CA, 90025, USA.
Gilad HalpertAriel University, Ari'el, Israel.
Yuri OstrinskiAriel University, Ari'el, Israel.ORCID http://orcid.org/0000-0001-9697-1554
Gabriela Crispim BaiocchiDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.ORCID http://orcid.org/0000-0003-0246-5883
Desirée Rodrigues PlaçaDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil.
Paula P FreireDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.ORCID http://orcid.org/0000-0003-0649-8279
Shahab Zaki PourLaboratory of Molecular Evolution and Bioinformatics, Department of Microbiology, Biomedical Sciences Institute, University of São Paulo, São Paulo, 05508-000, Brazil.ORCID http://orcid.org/0000-0002-7708-1406
Guido MollDepartament of Nephrology and Internal Intensive Care Medicine, Charité University Hospital, Berlin, Germany.ORCID http://orcid.org/0000-0001-6173-5957
Rusan CatarDepartament of Nephrology and Internal Intensive Care Medicine, Charité University Hospital, Berlin, Germany.
Yael Bublil LaviScakler faculty of medicine, Tel Aviv University, Tel Aviv, Israel.ORCID http://orcid.org/0000-0002-3162-0988
Jonathan I SilverbergDepartment of Dermatology, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
Jason ZimmermanMaimonides Medical Center, Brooklyn, NY, USA.
Gustavo Cabral-MirandaDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.
Robson F CarvalhoDepartment of Structural and Functional Biology, Institute of Biosciences, São Paulo State University (UNESP), Botucatu, São Paulo, Brazil.ORCID http://orcid.org/0000-0002-4901-7714
Taj Ali KhanInstitute of Pathology and Diagnostic Medicine, Khyber Medical University, Peshawar, Pakistan.
Harald HeideckeCellTrend Gesellschaft mit beschränkter Haftung (GmbH), Luckenwalde, Germany.
Rodrigo J S DalmolinBioinformatics Multidisciplinary Environment, Federal University of Rio Grande do Norte, Natal, Brazil.
Andre Ducati LuchessiDepartment of Clinical and Toxicological Analyses, Federal University of Rio Grande do Norte, R.N., Natal, Brazil.
Hans D OchsDepartment of Pediatrics, University of Washington School of Medicine, and Seattle Children's Research Institute, Seattle, WA, USA.
Lena F SchimkeDepartment of Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP, Brazil.ORCID http://orcid.org/0000-0002-5616-3410
Howard AmitalAriel University, Ari'el, Israel.
Gabriela RiemekastenDepartment of Rheumatology, University Medical Center Schleswig-Holstein Campus Lübeck, Lübeck, Germany.ORCID http://orcid.org/0000-0002-5406-2464
Israel Zyskind *Maimonides Medical Center, Brooklyn, NY, USA.ORCID http://orcid.org/0000-0003-3422-9631
Avi Z Rosenberg *Department of Pathology, Johns Hopkins University, Baltimore, MD, USA.ORCID http://orcid.org/0000-0003-2356-950X
Aristo Vojdani *Department of Immunology, Immunosciences Laboratory, Inc., Los Angeles, CA, USA.
Yehuda Shoenfeld *Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel.ORCID http://orcid.org/0000-0003-2802-4090
Otavio Cabral-Marques *Interunit Postgraduate Program on Bioinformatics, Institute of Mathematics and Statistics (IME), University of Sao Paulo (USP), Sao Paulo, SP, Brazil. otavio.cmarques@usp.br.ORCID http://orcid.org/0000-0002-3183-6236
Universidade de São Paulo · BRCharité - Universitätsmedizin Berlin · DEMaimonides Medical Center · USSt Petersburg University · RUTel Aviv University · ILUniversidade Federal do Rio Grande do Norte · BRGeorge Washington University · USGesellschaft für Klinische Forschung · DEImmunosciences Lab (United States) · USJohns Hopkins University · USKhyber Medical University · PKSeattle Children's Hospital · USSheba Medical Center · ILUniversidade Estadual Paulista (Unesp) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Age is a significant risk factor for the coronavirus disease 2019 (COVID-19) severity due to immunosenescence and certain age-dependent medical conditions (e.g., obesity, cardiovascular disorder, and chronic respiratory disease). However, despite the well-known influence of age on autoantibody biology in health and disease, its impact on the risk of developing severe COVID-19 remains poorly explored. Here, we performed a cross-sectional study of autoantibodies directed against 58 targets associated with autoimmune diseases in 159 individuals with different COVID-19 severity (71 mild, 61 moderate, and 27 with severe symptoms) and 73 healthy controls. We found that the natural production of autoantibodies increases with age and is exacerbated by SARS-CoV-2 infection, mostly in severe COVID-19 patients. Multiple linear regression analysis showed that severe COVID-19 patients have a significant age-associated increase of autoantibody levels against 16 targets (e.g., amyloid β peptide, β catenin, cardiolipin, claudin, enteric nerve, fibulin, insulin receptor a, and platelet glycoprotein). Principal component analysis with spectrum decomposition and hierarchical clustering analysis based on these autoantibodies indicated an age-dependent stratification of severe COVID-19 patients. Random forest analysis ranked autoantibodies targeting cardiolipin, claudin, and platelet glycoprotein as the three most crucial autoantibodies for the stratification of severe COVID-19 patients ≥50 years of age. Follow-up analysis using binomial logistic regression found that anti-cardiolipin and anti-platelet glycoprotein autoantibodies significantly increased the likelihood of developing a severe COVID-19 phenotype with aging. These findings provide key insights to explain why aging increases the chance of developing more severe COVID-19 phenotypes.

Identifiers

PMID37620330
PMCPMC10449916
OpenAlexW4386120045

What Socratic holds

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LicenceCC BY
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Registered trials

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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 Socratic graph.