Excessive inflammation triggered by a hitherto undescribed mechanism is a hallmark of severe SARS-CoV-2 infection and is associated with enhanced pathogenicity and mortality. Complement hyper activation promotes lung injury and was observed in patients suffering from MERS-CoV, SARS-CoV-1 and SARS-CoV-2 infections. To evaluate the very first interactions of SARS-CoV-2 patient isolates with human epithelial tissues, 3D models of the human respiratory tract as well as lung organoids are highly suitable.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- endothelial cells
- respiratory tract
- induced pluripotent stem cells
- end stage renal disease
- ejection fraction
- oxidative stress
- coronavirus disease
- newly diagnosed
- gene expression
- cardiovascular events
- escherichia coli
- risk factors
- coronary artery disease
- case report
- physical activity
- patient reported outcomes
- cardiovascular disease
- biofilm formation
- genetic diversity