tetano
Editor, Senior Moderator
Cell Stress Chaperones
. 2020 Aug 4.
doi: 10.1007/s12192-020-01148-3. Online ahead of print.
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[SUP] 1 [/SUP], S?bastien L?gar?[SUP] 2 3 [/SUP], Giosu? Lo Bosco[SUP] 4 [/SUP], Alberto Fucarino[SUP] 1 [/SUP], Francesca Angileri[SUP] 5 [/SUP], Everly Conway de Macario[SUP] 6 [/SUP], Alberto Jl Macario[SUP] 6 7 [/SUP], Francesco Cappello[SUP] 8 9 [/SUP]
Affiliations
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: Autoimmunity; COVID-19; Endothelialitis; Molecular chaperones; Molecular mimicry; Severe acute respiratory syndrome coronavirus 2.
. 2020 Aug 4.
doi: 10.1007/s12192-020-01148-3. Online ahead of print.
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[SUP] 1 [/SUP], S?bastien L?gar?[SUP] 2 3 [/SUP], Giosu? Lo Bosco[SUP] 4 [/SUP], Alberto Fucarino[SUP] 1 [/SUP], Francesca Angileri[SUP] 5 [/SUP], Everly Conway de Macario[SUP] 6 [/SUP], Alberto Jl Macario[SUP] 6 7 [/SUP], Francesco Cappello[SUP] 8 9 [/SUP]
Affiliations
- PMID: 32754823
- DOI: 10.1007/s12192-020-01148-3
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: Autoimmunity; COVID-19; Endothelialitis; Molecular chaperones; Molecular mimicry; Severe acute respiratory syndrome coronavirus 2.