Von Willebrand factor: A key glycoprotein involved in thrombo-inflammatory complications of COVID-19

Abstract

COVID-19 is an ongoing public health emergency that has affected millions of people worldwide and is still a threat to many more. One of the pathophysiological features of COVID-19 is associated with the activation of vascular endothelial cells (ECs) leading to the disruption of vascular integrity, coagulation and inflammation. An interlink mechanism between coagulation and inflammatory pathways has been reported in COVID-19. Multiple components are involved in these pathological pathways. Out of all, Von Willebrand Factor (VWF) is one of the primary components of coagulation pathway and also a mediator of vascular inflammation that plays an important role in thrombo-inflammation that further leads to acute respiratory distress syndrome (ARDS). The thrombo-inflammatory co-morbidities such as hyper-coagulation, thrombosis, ARDS etc. have become the major cause of mortality in the patients of COVID-19 admitted to the ICU. Thus, VWF can be explored as a potential target to manage COVID-19 associated co-morbidities. Supporting this hypothesis, there are literature reports which disclose previous attempts to target VWF for the management of thrombo-inflammation in other pathological conditions. The current report summarizes emerging insights into the pathophysiology, mechanism(s), diagnosis, management and foundations for research on this less explored clinically relevant glycoprotein as coagulation biomarker in COVID-19.

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

“…When endothelial dysfunction/endotheliopathy/endotheliitis occurs in COVID-19, several markers of endothelial cell activation are used for assessing endothelial dysfunction in COVID-19 (Figs. 4 and 5 ) [ 101 ].

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TEG®, Microclot and Platelet Mapping for Guiding Early Management of Severe COVID-19 Coagulopathy

“…From the vast literature in COVID-19 and clotting, it is now well-accepted that coagulopathies occur in the majority of patients who die from COVID-19 [35,36], and that DIC severe bleeding events are uncommon in COVID-19 patients [11]. However, COVID-19 can be complicated by DIC, which has a strongly prothrombotic character with a high risk of venous thromboembolism [26].…”

“…Selected References P-selectin [7,51] Fibrin(ogen) and D-dimer [38,42,45,47,[52][53][54][55][56][57][58]] Von Willebrand Factor [17,36,59,60] With the above-mentioned pathologies in mind, we here argue that the early treating of COVID-19 disease as a vascular and endothelial disease with severe platelet dysfunction and microclot formation, early on in the disease, provides a framework for a rational treatment strategy. We review literature on the use of point-of-care equipment such as the thromboelastography ® (TEG ® ) and the PFA200, to manage patient with COVID-19.…”

Relative Hypercoagulopathy of the SARS-CoV-2 Beta and Delta Variants when Compared to the Less Severe Omicron Variants Is Related to TEG Parameters, the Extent of Fibrin Amyloid Microclots, and the Severity of Clinical Illness

“…9 It is well established that the earlier variants (before omicron) caused severe disease and resulted in coagulopathies in critically ill patients. [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36] In contrast, the heavily mutated omicron variants have been shown to have milder symptoms than the earlier variants. The five most prevalent symptoms during omicron infection were reported to be runny nose, rhinitis headache, fatigue (either mild or severe), sneezing, and sore throat.…”