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From Anti-SARS-CoV-2 Immune Responses to COVID-19 via Molecular Mimicry.

ABSTRACT: AIM:To define the autoimmune potential of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. METHODS:Experimentally validated epitopes cataloged at the Immune Epitope DataBase (IEDB) and present in SARS-CoV-2 were analyzed for peptide sharing with the human proteome. RESULTS:Immunoreactive epitopes present in SARS-CoV-2 were mostly composed of peptide sequences present in human proteins that-when altered, mutated, deficient or, however, improperly functioning-may associate with a wide range of disorders, from respiratory distress to multiple organ failure. CONCLUSIONS:This study represents a starting point or hint for future scientific-clinical investigations and suggests a range of possible protein targets of autoimmunity in SARS-CoV-2 infection. From an experimental perspective, the results warrant the testing of patients' sera for autoantibodies against these protein targets. Clinically, the results warrant a stringent surveillance on the future pathologic sequelae of the current SARS-CoV-2 pandemic.

SUBMITTER: Kanduc D

PROVIDER: S-EPMC7551747 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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From Anti-SARS-CoV-2 Immune Responses to COVID-19 via Molecular Mimicry.

Kanduc Darja D

Antibodies (Basel, Switzerland) 20200716 3

<h4>Aim</h4>To define the autoimmune potential of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection.<h4>Methods</h4>Experimentally validated epitopes cataloged at the Immune Epitope DataBase (IEDB) and present in SARS-CoV-2 were analyzed for peptide sharing with the human proteome.<h4>Results</h4>Immunoreactive epitopes present in SARS-CoV-2 were mostly composed of peptide sequences present in human proteins that-when altered, mutated, deficient or, however, improperly funct ...[more]

PMID: 32708525

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Project description:BackgroundThe relationship between anti-SARS-CoV-2 humoral immune response, pathogenic inflammation, lymphocytes and fatal COVID-19 is poorly understood.MethodsA longitudinal prospective cohort of hospitalised patients with COVID-19 (n=254) was followed up to 35 days after admission (median, 8 days). We measured early anti-SARS-CoV-2 S1 antibody IgG levels and dynamic (698 samples) of quantitative circulating T-, B- and natural killer lymphocyte subsets and serum interleukin-6 (IL-6) response. We used machine learning to identify patterns of the immune response and related these patterns to the primary outcome of 28-day mortality in analyses adjusted for clinical severity factors.ResultsOverall, 45 (18%) patients died within 28 days after hospitalisation. We identified six clusters representing discrete anti-SARS-CoV-2 immunophenotypes. Clusters differed considerably in COVID-19 survival. Two clusters, the anti-S1-IgGlowestTlowestBlowestNKmodIL-6mod, and the anti-S1-IgGhighTlowBmodNKmodIL-6highest had a high risk of fatal COVID-19 (HR 3.36-21.69; 95% CI 1.51-163.61 and HR 8.39-10.79; 95% CI 1.20-82.67; p≤0.03, respectively). The anti-S1-IgGhighestTlowestBmodNKmodIL-6mod and anti-S1-IgGlowThighestBhighestNKhighestIL-6low cluster were associated with moderate risk of mortality. In contrast, two clusters the anti-S1-IgGhighThighBmodNKmodIL-6low and anti-S1-IgGhighestThighestBhighNKhighIL-6lowest clusters were characterised by a very low risk of mortality.ConclusionsBy employing unsupervised machine learning we identified multiple anti-SARS-CoV-2 immune response clusters and observed major differences in COVID-19 mortality between these clusters. Two discrete immune pathways may lead to fatal COVID-19. One is driven by impaired or delayed antiviral humoral immunity, independently of hyper-inflammation, and the other may arise through excessive IL-6-mediated host inflammation response, independently of the protective humoral response. Those observations could be explored further for application in clinical practice.

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From Anti-SARS-CoV-2 Immune Responses to COVID-19 via Molecular Mimicry.

Publications

From Anti-SARS-CoV-2 Immune Responses to COVID-19 via Molecular Mimicry.

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