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Physical phenotype of blood cells is altered in COVID-19


Senior Member

Clinical syndrome coronavirus disease 2019 (COVID-19) induced by severe acute respiratory syndrome coronavirus 2 is characterized by rapid spreading and high mortality worldwide. Although the pathology is not yet fully understood, hyperinflammatory response and coagulation disorders leading to congestions of microvessels are considered to be key drivers of the still-increasing death toll. Until now, physical changes of blood cells have not been considered to play a role in COVID-19 related vascular occlusion and organ damage. Here, we report an evaluation of multiple physical parameters including the mechanical features of five frequent blood cell types, namely erythrocytes, lymphocytes, monocytes, neutrophils, and eosinophils. More than four million blood cells of 17 COVID-19 patients at different levels of severity, 24 volunteers free from infectious or inflammatory diseases, and 14 recovered COVID-19 patients were analyzed. We found significant changes in lymphocyte stiffness, monocyte size, neutrophil size and deformability, and heterogeneity of erythrocyte deformation and size. Although some of these changes recovered to normal values after hospitalization, others persisted for months after hospital discharge, evidencing the long-term imprint of COVID-19 on the body.
One of the suggestions in the paper is that it could be cytokines making these changes to the immune cells. Makes sense. However i think another possibility might be the disrupted ephrin-eph pathway in me/cfs patients suggested in a 2021 paper by Arnaud Germain which is part of Maureen Hanson´s team. I dont know how that stuff works but my understanding is that this pathway is important for regulating the cytoskeleton.

The classic statistical approach, using a Wilcoxon test and multiple testing correction, highlighted nine proteins at a low false discovery rate (FDR) of q < 0.05, with one group linked to cellular structure through the cytoskeleton and the extracellular matrix, and a second group linked to the immune system. Of the three proteins related to cellular structure, AIF1L is involved in the cytoskeletal apparatus as an actin-bundling protein [24]. Al-though lower levels of AIF1L have been linked to poor prognosis during breast cancer, AIF1L overexpression in a cell line, similar to what is observed for our ME/CFS cohort (Table 2 and Figure 1), suppressed cell spreading and altered cell shape [25].


That said the current findings can explain tissue hypoxia without needing stuff like micro clots or autoantibodies so very interresting stuff.

edit: added the quote
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