PMC:7543426 / 11102-12515 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7543426","sourcedb":"PMC","sourceid":"7543426","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7543426","text":"A range of common lung findings were seen on light microscopy. Parenchymal multifocal damage with intraalveolar exudative and proliferative inflammation (Figure 1A2), with fibrin, hyaline membranes (Figure 1A3) consistent with a diagnosis of diffuse alveolar damage (Table 3). Organizing pneumonia with fibrosis and type II pneumocyte hyperplasia, amphophilic cytoplasm, large nuclei, and prominent nucleoli, were indicative of cytopathic virus-induced changes (Figure 1A3 and 1A4). Fibroblastic foci consisting of loose organizing connective tissue reflective of alveolar duct fibrosis were seen (fibrotic phase) (Figure 1B1). Other findings included: pleural fibrosis (Figure 1B4), vascular injury with thrombi (Figure 1B2), and vasculitis (Figure 1B3). A main feature was the presence of numerous inflammatory cells consisting of granulocytes (CD15+) (Supplementary Figure 1A1 and 1A2), macrophages (CD68+) (Supplementary Figure 1A3 and 1A4), and T lymphocytes (CD3+) infiltrating into alveolar septa and clustering around capillary vessels (Supplementary 1B1). Immunohistochemistry showed the presence of both CD4+ and CD8+ T lymphocytes (Supplementary Figure 1B2 and 1B3). Of note, lymphocytes were CD20− indicating an absence of infiltrating B lymphocytes. Thrombi were present and immunohistochemistry showed the presence of platelet aggregates and megakaryocytes within thrombi (Supplementary Figure 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