Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity agains
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SHORT COMMUNICATION
Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19 Antonella Marino Gammazza 1 & Sébastien Légaré 2,3 & Giosuè Lo Bosco 4 & Alberto Fucarino 1 & Francesca Angileri 5 & Everly Conway de Macario 6 & Alberto JL Macario 6,7 & Francesco Cappello 1,7 Received: 10 July 2020 / Revised: 27 July 2020 / Accepted: 30 July 2020 # Cell Stress Society International 2020
Abstract Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2), the cause of COVID-19 disease, has the potential to elicit autoimmunity because mimicry of human molecular chaperones by viral proteins. We compared viral proteins with human molecular chaperones, many of which are heat shock proteins, to determine if they share amino acid-sequence segments with immunogenic-antigenic potential, which can elicit cross-reactive antibodies and effector immune cells with the capacity to damage-destroy human cells by a mechanism of autoimmunity. We identified the chaperones that can putatively participate in molecular mimicry phenomena after SARS-CoV-2 infection, focusing on those for which endothelial cell plasma-cell membrane localization has already been demonstrated. We also postulate that post-translational modifications, induced by physical (shear) and chemical (metabolic) stress caused respectively by the risk factors hypertension and diabetes, might have a role in determining plasma-cell membrane localization and, in turn, autoimmune-induced endothelial damage. Keywords Severe acute respiratory syndrome coronavirus 2 . COVID-19 . Molecular chaperones . Molecular mimicry . Autoimmunity . Endothelialitis
Introduction Severe acute respiratory syndrome corona virus 2 (SARSCoV-2) causes COVID-19, a disease manifested with a wide spectrum of signs and symptoms, from a paucisymptomatic flu-like syndrome to a devastating multiorgan failure (MOF) (Wynants et al. 2020).
Histopathological lesions of the lungs were the first to be reported, but soon after similar morphological damages (mainly diffuse microthrombosis and disseminated intravascular coagulation or DIC) were found also in other organs, including liver, kidney, and brain (Sessa et al. 2020). Virtually all organs present these histological features that may have a common mechanism: endothelialitis due to an
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12192-020-01148-3) contains supplementary material, which is available to authorized users. * Francesco Cappello [email protected] 1
Department of Biomedicine, Neuroscience and Advanced Diagnostics (BIND), University of Palermo, Palermo, Italy
2
Département d’Informatique de l’ÉNS, ÉNS, CNRS, Université PSL, Paris, France
3
Centre de Recherche Inria de Paris, Paris, France
4
Department of Mathematics and Computer Science, University of Palermo, Palermo, Italy
5
Centre Léon Bérard, Cancer Research Center of Lyon, Université de Lyon, Un
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