A group from Karolinska University Laboratory, etc. has reported on their new findings from 12 patients autopsies where the direct cause of death was determined as COVID-19 associated ARDS.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8141733/
ARDS caused by COVID-19 appears to be the massive consolidation of the lung parenchyma. The process is initiated by virus replication in the pneumocytes leading to the desquamation of the alveolar epithelia and various levels of breach in the barriers between alveolar capillaries and the intra-alveolar space. With the increasing severity of this breach, edema fluid, plasma and eventually whole blood is leaking out into the alveolar space. Initiation of the coagulation cascade leads to the accumulation of fibrin filaments and/or intra-alveolar coagulated blood. Importantly only a minority of pneumocytes showed lytic virus replication but most pneumocytes in the affected area showed pronounced cytopathic effects in form of cytoplasmic swelling, vesicular degeneration and nuclear atypia.
Interestingly, the virus was replicating in the pneumocytes and macrophages but not in bronchial epithelium, endothelium, pericytes or stromal cells, suggesting that phagocytic cells consuming virus carrying cellular debris might themselves become infected, although the detailed mechanism is unknown.
The lung consolidation was accompanied with massive accumulation of CD163+ macrophages and immature myeloid elements, extensive proliferative response both in the epithelial and stromal components as well as exuberant neo-angiogenesis. The endothelial damage leading to the lung consolidation was considered to be caused by massive bystander effect, beyond the direct virus induced cytopathic damage, possibly induced by soluble factors such as ORF3a, inducing apoptosis in non-infected cells, released from the infected pneumocytes.