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SARS-CoV-2 infection as a trigger of humoral response against apolipoprotein A-1.

Division of Laboratory Medicine, Department of Diagnostics and of Medical Specialties, Geneva University Hospitals and Geneva University, Geneva, Switzerland. Centre for Vaccinology, Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland. Division of Intensive Care, Geneva University Hospitals and the University of Geneva Faculty of Medicine, Geneva, Switzerland. Faculty of Science, Department of Organic Chemistry, NCCR Chemical Biology, University of Geneva, Geneva, Switzerland. Division and Department of Primary Care Medicine, Geneva University Hospitals, Geneva, Switzerland. Faculty of BioMedicine, Università della Svizzera Italiana, Lugano, Switzerland. Faculty of Medicine, Department of Pathology and Immunology, University of Geneva, Switzerland. Faculty of Medicine, Departments of Pathology-Immunology and Pediatrics, University of Geneva, Geneva, Switzerland. Geneva Centre for Emerging Viral Diseases, Geneva University Hospitals, Geneva, Switzerland. Unit of Population Epidemiology, Division of Primary Care, Geneva University Hospitals, Geneva, Switzerland. Division of Infectious Diseases, Department of Medicine, Geneva University Hospitals, Geneva, Switzerland.

European journal of clinical investigation. 2021;(11):e13661
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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.