Abstract
Progressive respiratory failure is seen as a major cause of death in severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection. Relatively little is known about the associated morphologic and molecular changes in the circulation of these patients. In particular, platelet and erythrocyte pathology might result in severe vascular issues, and the manifestations may include thrombotic complications. These thrombotic pathologies may be both extrapulmonary and intrapulmonary and may be central to respiratory failure. Previously, we reported the presence of amyloid microclots in the circulation of patients with coronavirus disease 2019 (COVID-19). Here, we investigate the presence of related circulating biomarkers, including C-reactive protein (CRP), serum ferritin, and P-selectin. These biomarkers are well-known to interact with, and cause pathology to, platelets and erythrocytes. We also study the structure of platelets and erythrocytes using fluorescence microscopy (using the markers PAC-1 and CD62PE) and scanning electron microscopy. Thromboelastography and viscometry were also used to study coagulation parameters and plasma viscosity. We conclude that structural pathologies found in platelets and erythrocytes, together with spontaneously formed amyloid microclots, may be central to vascular changes observed during COVID-19 progression, including thrombotic microangiopathy, diffuse intravascular coagulation, and large-vessel thrombosis, as well as ground-glass opacities in the lungs. Consequently, this clinical snapshot of COVID-19 strongly suggests that it is also a true vascular disease and considering it as such should form an essential part of a clinical treatment regime.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, leading to coronavirus disease 2019 (COVID-19), is strongly associated with various coagulopathies that may result in thrombosis, thrombocytopenia, or bleeding in the later stages of the disease [1,2,3,4,5,6,7,8,9,10,11,12,13,14]
Diagnosed COVID-19 patient blood samples were collected, and the blood analysis reported here was done on treatment-naïve patients
We report extensive P-selectin signals on platelets from COVID-19 patients and, suggest that one reason might be because P-selectin is still present as an adhesion receptor attached to the platelet membrane, where it assists in platelet aggregation
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2)-induced infection, leading to coronavirus disease 2019 (COVID-19), is strongly associated with various coagulopathies that may result in thrombosis, thrombocytopenia, or bleeding in the later stages of the disease [1,2,3,4,5,6,7,8,9,10,11,12,13,14]. It is recognized that vascular changes and thrombotic microangiopathy, diffuse intravascular coagulation, and large-vessel thrombosis are major reasons for a poor prognosis [15]. These comorbidities are linked to multisystem organ failure, as well as pulmonary vascular endothelialitis [15]. In COVID-19, peripheral lung ground-glass opacities are an accompaniment in mild, moderate, and severe diseases, as visible on computed tomographic (CT) images. Peripheral lung ground-glass opacities in COVID-19 meet the Berlin criteria for acute respiratory distress syndrome (ARDS) [15]. We have found that amyloid fibrin(ogen) is a feature of a variety of inflammatory diseases [18,19,20,21,22,23]
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