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However, whether SARS-CoV-2 in the alveolar compartment is strictly ACE2-dependent and to what extent virus-induced tissue damage and\/or direct immune activation determines early pathogenesis is still elusive.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Spectral microscopy, single-cell\/-nucleus RNA sequencing or ACE2 \u201cgain-of-function\u201d experiments were applied to infected human lung explants and adult stem cell derived human lung organoids to correlate ACE2 and related host factors with SARS-CoV-2 tropism, propagation, virulence and immune activation compared to SARS-CoV, influenza and Middle East respiratory syndrome coronavirus (MERS-CoV). Coronavirus disease 2019 (COVID-19) autopsy material was used to validate<jats:italic>ex vivo<\/jats:italic>results.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We provide evidence that alveolar ACE2 expression must be considered scarce, thereby limiting SARS-CoV-2 propagation and virus-induced tissue damage in the human alveolus. Instead,<jats:italic>ex vivo<\/jats:italic>infected human lungs and COVID-19 autopsy samples showed that alveolar macrophages were frequently positive for SARS-CoV-2. Single-cell\/-nucleus transcriptomics further revealed nonproductive virus uptake and a related inflammatory and anti-viral activation, especially in \u201cinflammatory alveolar macrophages\u201d, comparable to those induced by SARS-CoV and MERS-CoV, but different from NL63 or influenza virus infection.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Collectively, our findings indicate that severe lung injury in COVID-19 probably results from a macrophage-triggered immune activation rather than direct viral damage of the alveolar compartment.<\/jats:p><\/jats:sec>","DOI":"10.1183\/13993003.02725-2021","type":"journal-article","created":{"date-parts":[[2022,6,22]],"date-time":"2022-06-22T00:45:23Z","timestamp":1655858723000},"page":"2102725","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":48,"title":["Human lungs show limited permissiveness for SARS-CoV-2 due to scarce ACE2 levels but 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