Inflammation and intussusceptive angiogenesis in COVID-19: everything in and out of flow
Maximilian Ackermann, Steven J. Mentzer, Martin Kolb, Danny Jonigk
Abstract
We recently showed that SARS-CoV-2 infection leads to angiocentric inflammation in COVID-19-induced respiratory failure, with a greater number of ACE2-positive endothelial cells compared to uninfected controls or to post mortem lung tissue from patients who succumbed to influenza A-related acute respiratory distress syndrome (ARDS) [1]. Although the detection of SARS-CoV-2 in post mortem tissue by transmission electron microscopy is a challenging task [4], replicated virus-like particles were observed enveloped in endothelial cells [1, 5] and lymphatic cells [6], and also in type 2 and 1 pneumocytes [6, 7]. Increasing clinical evidence shows that endothelial dysfunction is a common denominator after SARS-CoV-2 infection in the multi-organ complexity and severity of COVID-19 [3]. Inflammation and intussusceptive angiogenesis in COVID-19 <https://bit.ly/30lLh8K>