An Update on the Pathogenesis of COVID-19 and the Reportedly Rare Thrombotic Events Following Vaccination

Abstract

Today the coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has become a global health problem. After more than a year with the pandemic, although our knowledge has progressed on COVID-19, there are still many unknowns in virological, pathophysiological and immunological aspects. It is obvious that the most efficient solution to end this pandemic are safe and efficient vaccines. This manuscript summarizes the pathophysiological and thrombotic features of COVID-19 and the safety and efficacy of currently approved COVID-19 vaccines with an aim to clarify the recent concerns of thromboembolic events after COVID-19 vaccination. The influx of newer information is rapid, requiring periodic updates and objective assessment of the data on the pathogenesis of COVID-19 variants and the safety and efficacy of currently available vaccines.

New Portal Vein Thrombosis in Cirrhosis - is the Thrombophilia Exacerbated due to Vaccine or COVID-19?

“…However, the thrombotic perturbations uncovered in the COVID-19 era have critical relevance for patients with cirrhosis and surveillance for venous and arterial thromboembolism needs to be incorporated in clinical practice in the post COVID era. [ 7 ].…”

An Insight into the Role of Postmortem Immunohistochemistry in the Comprehension of the Inflammatory Pathophysiology of COVID-19 Disease and Vaccine-Related Thrombotic Adverse Events: A Narrative Review

“…The above considerations integrate the research in clinical settings performed on patients with severe vascular adverse reactions to the ChAdOx1 nCov-19 vaccine [ 38 , 39 ]. In fact, the more shared evaluation regarding the pathogenesis of vaccine-induced immune thrombotic thrombocytopenia (VITT) suggests that an adenoviral vector vaccine can trigger an immune response leading to highly reactive anti-PF4 (anti-platelet factor 4) antibodies activating platelets through their FcγRIIa receptors (CD32) [ 40 , 41 , 42 , 43 ]. Particularly, this receptor is distributed on several cells such as platelets, monocytes, macrophages, neutrophils, natural killer cells, and endothelial cells, and studies described specific CD32 polymorphism (i.e., 131 Arg-His heterozygous or 131-His-His homozygous phenotypes) associated with an enhanced activation of platelets in HIT [ 44 ].…”

Vaccination of adult patients living with chronic kidney disease against SARS-CoV-2: a position statement by the South African Nephrology Society

“…Of particular concern, given the hypercoagulable state that often accompanies CKD [6], is the risk of vaccine-induced thrombotic thrombocytopaenia (VITT). VITT has been predominantly described as a rare complication of the Oxford-AstraZeneca AZD1222/ChAdOx1 nCov-19 vaccine, but has also occurred in association with the Johnson & Johnson/Janssen Ad26.COV2.S vaccine, and most commonly affects women younger than 55 years of age [7]. It is thought that endothelial injury, induced by vaccine-derived spike protein, results in platelet factor (PF4) release; complexing of PF4 with endogenous heparan sulphate leads to a hapten-driven autoantibody response with a clinical presentation similar to that of type II heparin-induced thrombotic thrombocytopenia (HITT) [7].…”

“…VITT has been predominantly described as a rare complication of the Oxford-AstraZeneca AZD1222/ChAdOx1 nCov-19 vaccine, but has also occurred in association with the Johnson & Johnson/Janssen Ad26.COV2.S vaccine, and most commonly affects women younger than 55 years of age [7]. It is thought that endothelial injury, induced by vaccine-derived spike protein, results in platelet factor (PF4) release; complexing of PF4 with endogenous heparan sulphate leads to a hapten-driven autoantibody response with a clinical presentation similar to that of type II heparin-induced thrombotic thrombocytopenia (HITT) [7]. Although the risk of VITT in patients living with CKD is unknown, some reassurance may be drawn from the low prevalence of VITT in the general population, and the lack of apparent association of VITT with traditional venous or arterial thrombosis risk factors [7].…”