DOI: 10.37349/ei.2026.1003257 ISSN: 2768-6655

Potential molecular mimicry of proteins involved in atherogenesis and/or vasculitides with coronavirus antigens

Leonid P. Churilov, Victor S. Gurevich, Maria V. Muzalevskaya, Tatiana A. Novitskaya, Valeriia A. Shapkina, Polina A. Sobolevskaia, Vladimir J. Utekhin, Tamara V. Fedotkina, Muslimbek G. Normatov
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Aim: This study explores the pathogenesis of atherosclerosis, as well as the comorbidity of atherosclerosis and coronavirus infection. The objective of the article is to provide a rationale for the potential involvement of an autoimmune component in the observed comorbidity between these two conditions. Methods: The research utilized bioinformatic and laboratory techniques. The bioinformatic approach involved selecting 30 human autoantigens, either proven or hypothesized to participate in atherogenesis and/or arteritides, as well as the most immunogenic proteins from human coronavirus antigens. To identify shared minimal immunogenic determinants (pentapeptides) between human autoantigens and coronavirus antigens, the proprietary “Alignmentaj” program was employed. Antibody levels against apolipoprotein B-100 (ApoB-100) and Proteinase 3 (PR3) were measured using enzyme-linked immunosorbent assay (ELISA) in patients with cardiovascular disease following coronavirus disease 2019 (COVID-19). Post-mortem tissue samples were subjected to standard morphological examination, supplemented with immunohistochemical methods for pathomorphological analysis. Results: The analysis revealed that the spike protein of human coronaviruses exhibits the highest concentration of pentapeptides similar to those found in atherogenesis-associated proteins. Notably, ApoB-100 shared the greatest number of peptides. Post-COVID cardiovascular patients showed varied anti-ApoB antibody and anti-PR3 antibody levels and potential complications. Pathomorphological examination of the aorta and coronary arteries of patients who died from atherothrombotic complications following COVID-19 infection revealed signs of autoimmune inflammation. Lymphocytic infiltration, consisting of T-cells and B-cells, as well as indications of vasa vasorum vasculitis, were observed in areas of unstable aortic atherosclerotic plaques and in the adventitia of coronary arteries. Conclusions: The identified sequence homology between human coronavirus antigens and human autoantigens, together with laboratory data obtained from patients with cardiovascular pathology following COVID-19, supports the hypothesis that molecular mimicry contributes to the initiation or exacerbation of atherosclerotic cardiovascular disease in the post-COVID period.

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