Vascular angiogenesis distinguishes the pulmonary pathobiology of COVID-19 from that of equally severe influenza, according to autopsy reports published in the New England Journal of Medicine.
Lungs were obtained during autopsy from patients who died from COVID-19 (N=7), acute respiratory distress syndrome (ARDS) secondary to influenza A (H1N1) (N=7) or age-matched uninfected controls (N=10).
The histological pattern in lungs from patients who died from COVID-19 or influenza-associated respiratory failure was diffuse alveolar damage with perivascular T-cell infiltration.
Lungs from COVID-19 patients showed distinct vascular features, with diffuse necrosis of alveolar lining cells, pneumocyte type 2 hyperplasia, and linear intra-alveolar fibrin deposition.
Immunohistochemical analysis of angiotensin-converting enzyme 2 (ACE2) expression measured as mean relative counts per field of view were 0.25±0.14 and 0.35±0.15, for alveolar epithelial cells and 0.49±0.28 and 0.55±0.11, for endothelial cells from the lungs of COVID-19 and influenza patients respectively.
Severe endothelial injury was associated with the presence of intracellular virus, disrupted cell membranes and widespread thrombosis with microangiopathy. Alveolar capillary microthrombi were nine times more prevalent in patients with COVID-19 than in those with influenza. New vessel growth, predominantly intussusceptive angiogenesis, was 2.7 times as high in COVID-19 as patients with influenza.
The clinical implications of these findings requires further research.