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Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins

Antiphospholipid antibodies (aPL), assumed to cause antiphospholipid syndrome (APS), are notorious for their heterogeneity in targeting phospholipids and phospholipid-binding proteins. The persistent presence of Lupus anticoagulant and/or aPL against cardiolipin and/or β2-glycoprotein I have been sh...

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Autores principales: Emmenegger, Marc, Kumar, Sreedhar Saseendran, Emmenegger, Vishalini, Malinauskas, Tomas, Buettner, Thomas, Rose, Laura, Schierack, Peter, Sprinzl, Martin F., Sommer, Clemens J., Lackner, Karl J., Aguzzi, Adriano, Roggenbuck, Dirk, Frauenknecht, Katrin B. M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8673606/
https://www.ncbi.nlm.nih.gov/pubmed/34860860
http://dx.doi.org/10.1371/journal.ppat.1010118
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author Emmenegger, Marc
Kumar, Sreedhar Saseendran
Emmenegger, Vishalini
Malinauskas, Tomas
Buettner, Thomas
Rose, Laura
Schierack, Peter
Sprinzl, Martin F.
Sommer, Clemens J.
Lackner, Karl J.
Aguzzi, Adriano
Roggenbuck, Dirk
Frauenknecht, Katrin B. M.
author_facet Emmenegger, Marc
Kumar, Sreedhar Saseendran
Emmenegger, Vishalini
Malinauskas, Tomas
Buettner, Thomas
Rose, Laura
Schierack, Peter
Sprinzl, Martin F.
Sommer, Clemens J.
Lackner, Karl J.
Aguzzi, Adriano
Roggenbuck, Dirk
Frauenknecht, Katrin B. M.
author_sort Emmenegger, Marc
collection PubMed
description Antiphospholipid antibodies (aPL), assumed to cause antiphospholipid syndrome (APS), are notorious for their heterogeneity in targeting phospholipids and phospholipid-binding proteins. The persistent presence of Lupus anticoagulant and/or aPL against cardiolipin and/or β2-glycoprotein I have been shown to be independent risk factors for vascular thrombosis and pregnancy morbidity in APS. aPL production is thought to be triggered by–among other factors–viral infections, though infection-associated aPL have mostly been considered non-pathogenic. Recently, the potential pathogenicity of infection-associated aPL has gained momentum since an increasing number of patients infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been described with coagulation abnormalities and hyperinflammation, together with the presence of aPL. Here, we present data from a multicentric, mixed-severity study including three cohorts of individuals who contracted SARS-CoV-2 as well as non-infected blood donors. We simultaneously measured 10 different criteria and non-criteria aPL (IgM and IgG) by using a line immunoassay. Further, IgG antibody response against three SARS-CoV-2 proteins was investigated using tripartite automated blood immunoassay technology. Our analyses revealed that selected non-criteria aPL were enriched concomitant to or after an infection with SARS-CoV-2. Linear mixed-effects models suggest an association of aPL with prothrombin (PT). The strength of the antibody response against SARS-CoV-2 was further influenced by SARS-CoV-2 disease severity and sex of the individuals. In conclusion, our study is the first to report an association between disease severity, anti-SARS-CoV-2 immunoreactivity, and aPL against PT in patients with SARS-CoV-2.
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spelling pubmed-86736062021-12-16 Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins Emmenegger, Marc Kumar, Sreedhar Saseendran Emmenegger, Vishalini Malinauskas, Tomas Buettner, Thomas Rose, Laura Schierack, Peter Sprinzl, Martin F. Sommer, Clemens J. Lackner, Karl J. Aguzzi, Adriano Roggenbuck, Dirk Frauenknecht, Katrin B. M. PLoS Pathog Research Article Antiphospholipid antibodies (aPL), assumed to cause antiphospholipid syndrome (APS), are notorious for their heterogeneity in targeting phospholipids and phospholipid-binding proteins. The persistent presence of Lupus anticoagulant and/or aPL against cardiolipin and/or β2-glycoprotein I have been shown to be independent risk factors for vascular thrombosis and pregnancy morbidity in APS. aPL production is thought to be triggered by–among other factors–viral infections, though infection-associated aPL have mostly been considered non-pathogenic. Recently, the potential pathogenicity of infection-associated aPL has gained momentum since an increasing number of patients infected with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been described with coagulation abnormalities and hyperinflammation, together with the presence of aPL. Here, we present data from a multicentric, mixed-severity study including three cohorts of individuals who contracted SARS-CoV-2 as well as non-infected blood donors. We simultaneously measured 10 different criteria and non-criteria aPL (IgM and IgG) by using a line immunoassay. Further, IgG antibody response against three SARS-CoV-2 proteins was investigated using tripartite automated blood immunoassay technology. Our analyses revealed that selected non-criteria aPL were enriched concomitant to or after an infection with SARS-CoV-2. Linear mixed-effects models suggest an association of aPL with prothrombin (PT). The strength of the antibody response against SARS-CoV-2 was further influenced by SARS-CoV-2 disease severity and sex of the individuals. In conclusion, our study is the first to report an association between disease severity, anti-SARS-CoV-2 immunoreactivity, and aPL against PT in patients with SARS-CoV-2. Public Library of Science 2021-12-03 /pmc/articles/PMC8673606/ /pubmed/34860860 http://dx.doi.org/10.1371/journal.ppat.1010118 Text en © 2021 Emmenegger et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Emmenegger, Marc
Kumar, Sreedhar Saseendran
Emmenegger, Vishalini
Malinauskas, Tomas
Buettner, Thomas
Rose, Laura
Schierack, Peter
Sprinzl, Martin F.
Sommer, Clemens J.
Lackner, Karl J.
Aguzzi, Adriano
Roggenbuck, Dirk
Frauenknecht, Katrin B. M.
Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title_full Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title_fullStr Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title_full_unstemmed Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title_short Anti-prothrombin autoantibodies enriched after infection with SARS-CoV-2 and influenced by strength of antibody response against SARS-CoV-2 proteins
title_sort anti-prothrombin autoantibodies enriched after infection with sars-cov-2 and influenced by strength of antibody response against sars-cov-2 proteins
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8673606/
https://www.ncbi.nlm.nih.gov/pubmed/34860860
http://dx.doi.org/10.1371/journal.ppat.1010118
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