We assume that the synthetic S2P6 peptide and to a lesser extent the synthetic S1P4 peptide, could be of interest to measure the dynamic of antibody response to COVID-19 mRNA vaccines. The synthetic S2P6 peptide containing the spike residues 1138/1169 and to a lesser extent, the synthetic S1P4 peptide containing the spike residues 616/644 were recognized by the immune sera from comirnaty vaccine recipients but not COVID-19 recovered patients. In the present study, synthetic peptide-based ELISA assays were performed to identify linear B-cell epitopes into the spike protein that contribute to elicitation of antibody response in comirnaty-vaccinated individuals. The Pfizer-BioNTech COVID-19 vaccine comirnaty is a lipid nanoparticle-encapsulated mRNA encoding a full-length and prefusion-stabilized SARS-CoV-2 spike protein. The SARS-CoV-2 spike protein has been identified as the major antigen candidate for the development of COVID-19 vaccines. Considerable efforts have been devoted for the development of effective vaccine strategies against COVID-19.
The newly identified coronavirus SARS-CoV-2 is responsible for the worldwide pandemic COVID-19. Our findings illuminate COVID-19 pathogenesis and highlight the importance of considering autoimmune potential when developing therapeutic interventions to reduce adverse reactions. Antibodies cross-reacting with PRKG1 and tropomyosin may cause known COVID-19 complications such as blood-clotting disorders and cardiac disease, respectively. Another motif, ELDKY, is shared in multiple human proteins, such as PRKG1 involved in platelet activation and calcium regulation, and tropomyosin, which is linked to cardiac disease. Antibodies cross-reacting with thrombopoietin may induce thrombocytopenia, a condition observed in COVID-19 patients. We show that a TQLPP motif in Spike and thrombopoietin shares similar antibody binding properties. We discovered molecular mimicry hotspots in Spike and highlight two examples with tentative high autoimmune potential and implications for understanding COVID-19 complications. Thus, we computationally investigated molecular mimicry between SARS-CoV-2 Spike and known epitopes. Autoimmunity due to cross-reacting antibodies resulting from molecular mimicry between viral antigens and host proteins may provide an explanation. The coronavirus SARS-CoV-2 causes COVID-19, a disease curiously resulting in varied symptoms and outcomes, ranging from asymptomatic to fatal. Molecular mimicry between viral antigens and host proteins can produce cross-reacting antibodies leading to autoimmunity.
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