COVID-19 Vaccination with Special Reference to Adenoviral Vectors, Clotting Disorders and Old Age

Sergei V. Jargin
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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
COVID-19疫苗接种特别涉及腺病毒载体、凝血障碍和老年
关于COVID-19疫苗接种潜在副作用的统计数据的可靠性值得怀疑;不良反应可能被忽略,归因于其他原因或混淆。在这种情况下,基于病理生理生化机制的理论论证的作用越来越大。例如,在COVID-19患者中观察到的刺突蛋白(SP)的作用,在注射含有SP(灭活病毒疫苗)的疫苗或诱导细胞合成SP的核酸后,也可能在一定程度上发生。SP可通过下调血管紧张素转换酶2 (angiotensinconverting enzyme 2, ACE2)从而抑制线粒体功能,从而损害血管内皮细胞。SARS-CoV-2使用ACE2作为细胞受体,这可能导致ACE2降解和血管紧张素ii介导的COVID-19肺损伤。SP被呈递给免疫系统,诱导免疫反应,并与血小板上的ACE2受体结合,使其活化。内皮损伤和血小板活化会导致血栓形成和血小板减少,完全表达为疫苗诱导的血栓性血小板减少[12]。值得注意的是,疫苗后凝血障碍患者的D -二聚体水平通常较高[12,13]。血栓形成和血小板减少症不仅可能由SP引起,也可能由疫苗中的腺病毒载体[14]引起。载体引发细胞和体液免疫反应,与循环血小板结合,诱导其激活和聚集。有证据支持SP和腺病毒载体在疫苗中的协同作用。这些机制可能解释了应用基于腺病毒载体的抗sars - cov -2疫苗后血栓形成和血小板减少的相对较高患病率,例如脑和内脏静脉血栓形成、肺栓塞和弥散性血管内凝血[14]。此外,SP在体外已被证明可以进入细胞核并损害DNA修复[15],这可能会在未来产生深远的影响。给编辑的信
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