Abstract
By examining the issue of the thromboses and hemostasis disorders associated with severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) through the lens of cross-reactivity, it was found that 60 pentapeptides are shared by SARS-CoV-2 spike glycoprotein (gp) and human proteins that— when altered, mutated, deficient or, however, improperly functioning— cause vascular diseases, thromboembolic complications, venous thrombosis, thrombocytopenia, coagulopathies, and bleeding, inter alia. The peptide commonality has a relevant immunological potential as almost all of the shared sequences are present in experimentally validated SARS-CoV-2 spike gp-derived epitopes, thus supporting the possibility of cross-reactions between the viral gp and the thromboses-related human proteins. Moreover, many of the shared peptide sequences are also present in pathogens to which individuals have previously been exposed following natural infection or vaccinal routes, and of which the immune system has stored imprint. Such an immunological memory might rapidly trigger anamnestic secondary cross-reactive responses of extreme affinity and avidity, in this way explaining the thromboembolic adverse events that can associate with SARS-CoV-2 infection or active immunization.
Highlights
Clinical studies have shown that severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection can lead to an increased incidence of disorders such as thrombosis, venous thrombosis, and pulmonary embolism.[1,2,3]
A main conclusion of these studies is that, it cannot be proven that the hypercoagulable state is a direct causative effect of SARS-CoV-2 infection, it is apparent that patients with SARS-CoV-2 could have a predilection to the occurrence of thromboembolic events.[1]
The immunological potential of the peptides shared between SARS-CoV-2 spike gp and thrombosis-related proteins was analyzed by searching the Immune Epitope DataBase (IEDB [www.iedb.org/])[10] for immunoreactive SARS-CoV-2 spike gp-derived epitopes hosting the shared pentaptides
Summary
Clinical studies have shown that severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection can lead to an increased incidence of disorders such as thrombosis, venous thrombosis, and pulmonary embolism.[1,2,3] A main conclusion of these studies is that, it cannot be proven that the hypercoagulable state is a direct causative effect of SARS-CoV-2 infection, it is apparent that patients with SARS-CoV-2 could have a predilection to the occurrence of thromboembolic events.[1]. Currently there are no hypotheses or data that might suggest a molecular mechanism that relates to such SARS-CoV-2-related thromboembolic events. Searching for possible mechanisms, the present study analyzes the SARSCoV-2 spike glycoprotein (gp) for peptide sharing, that is, molecular mimicry, with human proteins, alterations of which may cause thromboses and hemostasis diseases. The underlying scientific rationale is that peptides common to a pathogen and the human host may lead to autoimmune pathologies through cross-reactivity phenomena following pathogen infection.[4,5,6] The results indicate that several linear
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