Spotlight on COVID-19 and Endothelial Damage
Coronavirus Disease 2019 (COVID-19) infects host cells through the binding of the spike (S) glycoprotein of the SARS-CoV-2 to ACE2 causing damage in vascular endothelium. Reduction of ACE2 to limit infection led to a dysfunctional endothelium as the protective effects of ACE were lost.
Fibrosis and COVID-19
Researchers have identified a unique COVID-19 signature in the lung, the mechanisms of which are contributors towards fibrosis.
ACE2 contributes to the maintenance of mouse epithelial barrier function
A recent COVID-19 study has utilised organoids to look into the effects of deleting ACE2, the protein which the virus uses to enter the cell.
SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells and is detected in specific cell subsets across tissues
A recent study has used single-cell RNA-seq data to analyse human, non-human primate and mouse barrier tissue to identify putative SARS-CoV-2 targets.
Immune cell proﬁling of COVID-19 patients in the recovery stage by single-cell sequencing
Authors of a recent COVID-19 study have applied single cell sequencing to characterise the immune cell repertoire and gene expression changes in recovering patients.