Physical phenotype of blood cells is altered in COVID-19

Abstract

Clinical syndrome coronavirus disease 2019 (COVID-19) induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is characterized by rapid spreading and high mortality worldwide. While the pathology is not yet fully understood, hyper-inflammatory 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 4 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. While 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.

A Fungal Defensin Targets the SARS−CoV−2 Spike Receptor−Binding Domain

“…Because the membrane−disruptive activity in many cases lacks a cellular specificity, it is likely that such permeabilization would also occur in erythrocytes. If it is true, this finding might well explain the recently observed physical phenotype alterations in blood cells of COVID−19 patients [ 52 ]. Therefore, further screening and engineering of fungus−derived high−affinity binders to block the Spike protein could be of value in exploiting drugs to relieve the Spike protein−evoked symptoms of COVID−19.…”

The Role of Alveolar Edema in COVID-19

“…Moreover, the pulmonary hypertension and the subsequent right ventricular dysfunction also have been confirmed in severe COVID-19 patients (Table 1) [39,40]. Significant alternations in monocyte size, lymphocyte stiffness, neutrophil size and deformability, and heterogeneity of erythrocyte size and deformation in COVID-19 patients also indicated great changes in pulmonary blood stream dynamics [41].…”

“…[36][37][38] General pulmonary vasoconstriction Lead to pulmonary hypertension and a risk of right-heart failure subsequently. [39][40][41] Severe ventilation-perfusion mismatch Induce hypoxemia in the non-injured fraction or/and cause hyper-perfusion of the small injured fraction. [42,43] Intravascular coagulation and microthrombi formation Lead to increased wasted ventilation and less efficient carbon dioxide removal.…”

Severe acute respiratory syndrome coronavirus 2 and respiratory syncytial virus coinfection in children

“…Molecular and serological tests are recommended by the Centers for Disease Control and Prevention to diagnose patients with SARS-CoV-2 infection. COVID-19 can result in significant alterations in the white blood cell count, elevated number of neutrophils and decreased number of lymphocytes have been reported in patients with severe COVID-19 [ 52 ]. Some laboratory predictors of COVID-19 have been identified in children, including increased or decreased levels of markers such as procalcitonin, D-dimer, and creatine kinase, as well as elevated liver enzymes [ 41 ].…”