{"title":"COVID-19 Vaccination with Special Reference to Adenoviral Vectors, Clotting Disorders and Old Age","authors":"Sergei V. Jargin","doi":"10.13188/2373-1133.1000023","DOIUrl":null,"url":null,"abstract":"Statistics about potential side effects of COVID-19 vaccination are of questionable reliability; adverse effects may be missed, ascribed to other causes or obfuscated. Under these circumstances, the role of theoretic argumentation based on patho physiological and biochemical mechanisms increases. For example, effects of the spike protein (SP) observed in COVID-19 patients can be expected to occur to some extent also after injections of vaccines containing SP (inactivated viral vaccines) or nucleic acids inducing the synthesis of SP by cells. SP can damage vascular endothelial cells by down regulating angiotensinconverting enzyme 2 (ACE2) and consequently inhibiting mitochondrial function [10]. SARS-CoV-2 uses ACE2 as a cellular receptor, which may lead to the ACE2 degradation and angiotensinII-mediated lung injury in COVID-19 [11]. SP is presented to the immune system inducing immune reactions and binds to ACE2 receptors on platelets activating them [11]. The endothelial damage together with the platelet activation would result in thromboses and thrombocytopenia wholly expressed in the entity known as vaccineinduced thrombotic thrombocytopenia [12]. Of note, D‐dimer level is usually high in patients with postvaccinal clotting disorders [12,13]. Thrombosis and thrombocytopenia may be caused not only by SP but also by adenoviral vectors in vaccines [14]. The vectors elicit cellular and humoral immune responses, bind to circulating platelets, inducing their activation and aggregation. There is evidence in favor of synergistic effects of SP and adenoviral vector in vaccines. These mechanisms may explain the comparatively high prevalence of thromboses and thrombocytopenia following application of adenoviral vector-based anti-SARS-CoV-2 vaccines e.g. cerebral and splanchnic vein thrombosis, pulmonary embolism and disseminated intravascular coagulation [14]. Moreover, SP has been shown in vitro to enter cell nuclei and to impair DNA repair [15], which may have far-reaching consequences to be studied in future. Letter to the Editor","PeriodicalId":90595,"journal":{"name":"Journal of geriatrics and palliative care","volume":"25 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of geriatrics and palliative care","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.13188/2373-1133.1000023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1
Abstract
Statistics about potential side effects of COVID-19 vaccination are of questionable reliability; adverse effects may be missed, ascribed to other causes or obfuscated. Under these circumstances, the role of theoretic argumentation based on patho physiological and biochemical mechanisms increases. For example, effects of the spike protein (SP) observed in COVID-19 patients can be expected to occur to some extent also after injections of vaccines containing SP (inactivated viral vaccines) or nucleic acids inducing the synthesis of SP by cells. SP can damage vascular endothelial cells by down regulating angiotensinconverting enzyme 2 (ACE2) and consequently inhibiting mitochondrial function [10]. SARS-CoV-2 uses ACE2 as a cellular receptor, which may lead to the ACE2 degradation and angiotensinII-mediated lung injury in COVID-19 [11]. SP is presented to the immune system inducing immune reactions and binds to ACE2 receptors on platelets activating them [11]. The endothelial damage together with the platelet activation would result in thromboses and thrombocytopenia wholly expressed in the entity known as vaccineinduced thrombotic thrombocytopenia [12]. Of note, D‐dimer level is usually high in patients with postvaccinal clotting disorders [12,13]. Thrombosis and thrombocytopenia may be caused not only by SP but also by adenoviral vectors in vaccines [14]. The vectors elicit cellular and humoral immune responses, bind to circulating platelets, inducing their activation and aggregation. There is evidence in favor of synergistic effects of SP and adenoviral vector in vaccines. These mechanisms may explain the comparatively high prevalence of thromboses and thrombocytopenia following application of adenoviral vector-based anti-SARS-CoV-2 vaccines e.g. cerebral and splanchnic vein thrombosis, pulmonary embolism and disseminated intravascular coagulation [14]. Moreover, SP has been shown in vitro to enter cell nuclei and to impair DNA repair [15], which may have far-reaching consequences to be studied in future. Letter to the Editor