Despite widespread interest in the pathophysiology of the Covid-19 disease, relatively little is known. In this study, we examined the morphologic and molecular features of seven lungs obtained during autopsy from patients who died from SARS- CoV-2 infection and it were compared with those obtained during autopsy from patients who had died from ARDS secondary to influenza A(H1N1) infection and from uninfected controls. The lungs were studied with the use of seven-color immunohistochemical analysis, micro–computed tomographic imaging, scanning electron microscopy, corrosion casting, and direct multiplexed measurement of gene expression. The lungs from the patients with Covid-19 and the patients with influenza shared a common morphologic pattern of diffuse alveolar damage and infiltrating perivascular lymphocytes. There were three distinctive angiocentric features of Covid-19: severe endothelial injury associated with intracellular SARS-CoV-2 virus and disrupted endothelial cell membranes, the lungs had widespread vascular thrombosis with microangiopathy and occlusion of alveolar capillaries and the lungs had significant new vessel growth through a mechanism of intussusceptive angiogenesis. Although the major limitation is that the sample was small, the vascular angiogenesis distinguished the pulmonary pathobiology of Covid-19 from that of equally severe influenza virus infection. The relationship of these findings to the clinical course of Covid-19 requires further research to elucidate. To aid others in their research, our full data set is available on the Vivli platform (https:// vivli.org/).