SARS‐CoV‐2 infection as a trigger of humoral response against apolipoprotein A‐1
Background Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. We aimed at determining (a) the association between anti‐SARS‐C...
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Published in | European journal of clinical investigation Vol. 51; no. 11; pp. e13661 - n/a |
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Main Authors | , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford
Blackwell Publishing Ltd
01.11.2021
John Wiley and Sons Inc |
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Abstract | Background
Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. We aimed at determining (a) the association between anti‐SARS‐CoV‐2 and anti‐apoA‐1 humoral response and (b) the degree of linear homology between SARS‐CoV‐2, apoA‐1 and Toll‐like receptor 2 (TLR2) epitopes.
Design
Bioinformatics modelling coupled with mimic peptides engineering and competition experiments were used to assess epitopes sequence homologies. Anti‐SARS‐CoV‐2 and anti‐apoA‐1 IgG as well as cytokines were assessed by immunoassays on a case‐control (n = 101), an intensive care unit (ICU; n = 126) and a general population cohort (n = 663) with available samples in the pre and post‐pandemic period.
Results
Using bioinformatics modelling, linear sequence homologies between apoA‐1, TLR2 and Spike epitopes were identified but without experimental evidence of cross‐reactivity. Overall, anti‐apoA‐1 IgG levels were higher in COVID‐19 patients or anti‐SARS‐CoV‐2 seropositive individuals than in healthy donors or anti‐SARS‐CoV‐2 seronegative individuals (P < .0001). Significant and similar associations were noted between anti‐apoA‐1, anti‐SARS‐CoV‐2 IgG, cytokines and lipid profile. In ICU patients, anti‐SARS‐CoV‐2 and anti‐apoA‐1 seroconversion rates displayed similar 7‐day kinetics, reaching 82% for anti‐apoA‐1 seropositivity. In the general population, SARS‐CoV‐2‐exposed individuals displayed higher anti‐apoA‐1 IgG seropositivity rates than nonexposed ones (34% vs 16.8%; P = .004).
Conclusion
COVID‐19 induces a marked humoral response against the major protein of high‐density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long‐term COVID‐19 prognosis assessment and warrant further scrutiny in the current COVID‐19 pandemic. |
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AbstractList | Background
Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. We aimed at determining (a) the association between anti‐SARS‐CoV‐2 and anti‐apoA‐1 humoral response and (b) the degree of linear homology between SARS‐CoV‐2, apoA‐1 and Toll‐like receptor 2 (TLR2) epitopes.
Design
Bioinformatics modelling coupled with mimic peptides engineering and competition experiments were used to assess epitopes sequence homologies. Anti‐SARS‐CoV‐2 and anti‐apoA‐1 IgG as well as cytokines were assessed by immunoassays on a case‐control (n = 101), an intensive care unit (ICU; n = 126) and a general population cohort (n = 663) with available samples in the pre and post‐pandemic period.
Results
Using bioinformatics modelling, linear sequence homologies between apoA‐1, TLR2 and Spike epitopes were identified but without experimental evidence of cross‐reactivity. Overall, anti‐apoA‐1 IgG levels were higher in COVID‐19 patients or anti‐SARS‐CoV‐2 seropositive individuals than in healthy donors or anti‐SARS‐CoV‐2 seronegative individuals (P < .0001). Significant and similar associations were noted between anti‐apoA‐1, anti‐SARS‐CoV‐2 IgG, cytokines and lipid profile. In ICU patients, anti‐SARS‐CoV‐2 and anti‐apoA‐1 seroconversion rates displayed similar 7‐day kinetics, reaching 82% for anti‐apoA‐1 seropositivity. In the general population, SARS‐CoV‐2‐exposed individuals displayed higher anti‐apoA‐1 IgG seropositivity rates than nonexposed ones (34% vs 16.8%; P = .004).
Conclusion
COVID‐19 induces a marked humoral response against the major protein of high‐density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long‐term COVID‐19 prognosis assessment and warrant further scrutiny in the current COVID‐19 pandemic. BackgroundUnravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. We aimed at determining (a) the association between anti‐SARS‐CoV‐2 and anti‐apoA‐1 humoral response and (b) the degree of linear homology between SARS‐CoV‐2, apoA‐1 and Toll‐like receptor 2 (TLR2) epitopes.DesignBioinformatics modelling coupled with mimic peptides engineering and competition experiments were used to assess epitopes sequence homologies. Anti‐SARS‐CoV‐2 and anti‐apoA‐1 IgG as well as cytokines were assessed by immunoassays on a case‐control (n = 101), an intensive care unit (ICU; n = 126) and a general population cohort (n = 663) with available samples in the pre and post‐pandemic period.ResultsUsing bioinformatics modelling, linear sequence homologies between apoA‐1, TLR2 and Spike epitopes were identified but without experimental evidence of cross‐reactivity. Overall, anti‐apoA‐1 IgG levels were higher in COVID‐19 patients or anti‐SARS‐CoV‐2 seropositive individuals than in healthy donors or anti‐SARS‐CoV‐2 seronegative individuals (P < .0001). Significant and similar associations were noted between anti‐apoA‐1, anti‐SARS‐CoV‐2 IgG, cytokines and lipid profile. In ICU patients, anti‐SARS‐CoV‐2 and anti‐apoA‐1 seroconversion rates displayed similar 7‐day kinetics, reaching 82% for anti‐apoA‐1 seropositivity. In the general population, SARS‐CoV‐2‐exposed individuals displayed higher anti‐apoA‐1 IgG seropositivity rates than nonexposed ones (34% vs 16.8%; P = .004).ConclusionCOVID‐19 induces a marked humoral response against the major protein of high‐density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long‐term COVID‐19 prognosis assessment and warrant further scrutiny in the current COVID‐19 pandemic. Abstract Background Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the development of potential therapeutic candidate targets and prognostic tools. We aimed at determining (a) the association between anti‐SARS‐CoV‐2 and anti‐apoA‐1 humoral response and (b) the degree of linear homology between SARS‐CoV‐2, apoA‐1 and Toll‐like receptor 2 (TLR2) epitopes. Design Bioinformatics modelling coupled with mimic peptides engineering and competition experiments were used to assess epitopes sequence homologies. Anti‐SARS‐CoV‐2 and anti‐apoA‐1 IgG as well as cytokines were assessed by immunoassays on a case‐control (n = 101), an intensive care unit (ICU; n = 126) and a general population cohort (n = 663) with available samples in the pre and post‐pandemic period. Results Using bioinformatics modelling, linear sequence homologies between apoA‐1, TLR2 and Spike epitopes were identified but without experimental evidence of cross‐reactivity. Overall, anti‐apoA‐1 IgG levels were higher in COVID‐19 patients or anti‐SARS‐CoV‐2 seropositive individuals than in healthy donors or anti‐SARS‐CoV‐2 seronegative individuals ( P < .0001). Significant and similar associations were noted between anti‐apoA‐1, anti‐SARS‐CoV‐2 IgG, cytokines and lipid profile. In ICU patients, anti‐SARS‐CoV‐2 and anti‐apoA‐1 seroconversion rates displayed similar 7‐day kinetics, reaching 82% for anti‐apoA‐1 seropositivity. In the general population, SARS‐CoV‐2‐exposed individuals displayed higher anti‐apoA‐1 IgG seropositivity rates than nonexposed ones (34% vs 16.8%; P = .004). Conclusion COVID‐19 induces a marked humoral response against the major protein of high‐density lipoproteins. As a correlate of poorer prognosis in other clinical settings, such autoimmunity signatures may relate to long‐term COVID‐19 prognosis assessment and warrant further scrutiny in the current COVID‐19 pandemic. |
Author | Kaiser, Laurent Yerly, Sabine Hartley, Oliver Farrera‐Soler, Lluc Vuilleumier, Nicolas Piumatti, Giovanni Guessous, Idris Eberhardt, Christiane S. Daguer, Jean‐Pierre Winssinger, Nicolas Pagano, Sabrina Stringhini, Silvia Meyer, Benjamin Le Terrier, Christophe Juillard, Catherine Eckerle, Isabella Siegrist, Claire‐Anne Suh, Noémie Lemaitre, Barbara Barluenga, Sofia Pugin, Jerome |
AuthorAffiliation | 2 Centre for Vaccinology Department of Pathology and Immunology University of Geneva Geneva Switzerland 7 Faculty of Medicine Department of Pathology and Immunology University of Geneva Switzerland 10 Unit of Population Epidemiology Division of Primary Care Geneva University Hospitals Geneva Switzerland 4 Faculty of Science Department of Organic Chemistry NCCR Chemical Biology University of Geneva Geneva Switzerland 5 Division and Department of Primary Care Medicine Geneva University Hospitals Geneva Switzerland 3 Division of Intensive Care Geneva University Hospitals and the University of Geneva Faculty of Medicine Geneva Switzerland 9 Geneva Centre for Emerging Viral Diseases Geneva University Hospitals Geneva Switzerland 1 Division of Laboratory Medicine Department of Diagnostics and of Medical Specialties Geneva University Hospitals and Geneva University Geneva Switzerland 6 Faculty of BioMedicine Università della Svizzera Italiana Lugano Switzerland 8 Faculty of Medicine Departments of Pat |
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CitedBy_id | crossref_primary_10_3389_fcvm_2024_1343361 crossref_primary_10_1111_eci_13818 crossref_primary_10_3389_fphar_2022_936659 crossref_primary_10_1111_eci_13729 crossref_primary_10_3389_fimmu_2023_1154058 crossref_primary_10_3390_vaccines11030670 crossref_primary_10_1111_eci_13713 crossref_primary_10_3389_fmed_2024_1357659 |
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Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the... Abstract Background Unravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and... BackgroundUnravelling autoimmune targets triggered by SARS‐CoV‐2 infection may provide crucial insights into the physiopathology of the disease and foster the... BACKGROUNDUnravelling autoimmune targets triggered by SARS-CoV-2 infection may provide crucial insights into the physiopathology of the disease and foster the... |
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SubjectTerms | anti‐apolipoprotein A‐1 autoantibodies Apolipoprotein A Autoimmunity Bioinformatics COVID-19 Cytokines Epitopes Homology Immune response (humoral) Immunoassays Immunoglobulin G Infections Lipids Lipoproteins Modelling molecular mimicry Original Pandemics Patients Peptides Prognosis Seroconversion Severe acute respiratory syndrome Severe acute respiratory syndrome coronavirus 2 spike protein TLR2 protein Toll-like receptors toll‐like receptor 2 Viral diseases |
Title | SARS‐CoV‐2 infection as a trigger of humoral response against apolipoprotein A‐1 |
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