Abstract:
Higher thrombotic burden in the acute phase of COVID-19 relies on a complex interplay
between pro-inflammatory cytokine/chemokine release, increased endothelial dysfunction/
damage, and potential sepsis-induced coagulopathy development in severe cases, all
promoting coagulation activation. Plasma levels of cytokines and chemokines are known to
be increased in COVID-19 however, are much higher in severe infections. Increased levels of IL1β, IL-6, and IL-8 are known to play an important role in both acute and chronic inflammation,
resulting in pathological clotting. However, little has been published on the effects of these
interleukins on red blood cells (RBCs). Evidence shows that cytokines have a negative effect on
the RBCs ultrastructure and introduce signs of eryptosis. Eryptosis can be described as a form
of suicidal death of RBCs characterized by distinct findings of cell shrinkage, membrane
blebbing, activation of proteases, and phosphatidylserine exposure at the outer membrane
leaflet. Red blood cells from COVID-19 patients had increased levels of glycolytic intermediates,
accompanied by oxidation and fragmentation of ankyrin, spectrin beta, and the N-terminal
cytosolic domain of band 3 (AE1). Significantly altered lipid metabolism was also observed, in
particular, short- and medium-chain saturated fatty acids, acyl-carnitines, and sphingolipids.
Emerging research suggests that RBCs may contribute to a precision medicine approach to
sepsis and have diagnostic value in monitoring complement dysregulation in COVID-19-sepsis
and non-COVID sepsis as research indicates that complement activation products and viral
antigens are present on RBCs in patients with COVID-19.
