PMC:7252096 / 165-1339 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T26168","span":{"begin":188,"end":195},"obj":"Body_part"},{"id":"T3086","span":{"begin":304,"end":310},"obj":"Body_part"},{"id":"T96149","span":{"begin":362,"end":366},"obj":"Body_part"},{"id":"T2013","span":{"begin":406,"end":413},"obj":"Body_part"},{"id":"T71632","span":{"begin":537,"end":541},"obj":"Body_part"},{"id":"T11","span":{"begin":542,"end":545},"obj":"Body_part"},{"id":"T53995","span":{"begin":652,"end":658},"obj":"Body_part"},{"id":"T53830","span":{"begin":668,"end":672},"obj":"Body_part"},{"id":"T64083","span":{"begin":725,"end":730},"obj":"Body_part"},{"id":"T86971","span":{"begin":738,"end":742},"obj":"Body_part"},{"id":"T26959","span":{"begin":751,"end":762},"obj":"Body_part"},{"id":"T62780","span":{"begin":781,"end":792},"obj":"Body_part"},{"id":"T95195","span":{"begin":821,"end":826},"obj":"Body_part"},{"id":"T65890","span":{"begin":897,"end":901},"obj":"Body_part"},{"id":"T10275","span":{"begin":930,"end":946},"obj":"Body_part"},{"id":"T33745","span":{"begin":941,"end":946},"obj":"Body_part"},{"id":"T94008","span":{"begin":1106,"end":1112},"obj":"Body_part"},{"id":"T5618","span":{"begin":1140,"end":1144},"obj":"Body_part"}],"attributes":[{"id":"A19641","pred":"fma_id","subj":"T26168","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A5895","pred":"fma_id","subj":"T3086","obj":"http://purl.org/sig/ont/fma/fma82764"},{"id":"A94439","pred":"fma_id","subj":"T96149","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A9231","pred":"fma_id","subj":"T2013","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A41093","pred":"fma_id","subj":"T71632","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A37948","pred":"fma_id","subj":"T11","obj":"http://purl.org/sig/ont/fma/fma67095"},{"id":"A29828","pred":"fma_id","subj":"T53995","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A91950","pred":"fma_id","subj":"T53830","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A90231","pred":"fma_id","subj":"T64083","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A42000","pred":"fma_id","subj":"T86971","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A95827","pred":"fma_id","subj":"T26959","obj":"http://purl.org/sig/ont/fma/fma62499"},{"id":"A57621","pred":"fma_id","subj":"T62780","obj":"http://purl.org/sig/ont/fma/fma62122"},{"id":"A22036","pred":"fma_id","subj":"T95195","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A44988","pred":"fma_id","subj":"T65890","obj":"http://purl.org/sig/ont/fma/fma74402"},{"id":"A15878","pred":"fma_id","subj":"T10275","obj":"http://purl.org/sig/ont/fma/fma66768"},{"id":"A11400","pred":"fma_id","subj":"T33745","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A53972","pred":"fma_id","subj":"T94008","obj":"http://purl.org/sig/ont/fma/fma9637"},{"id":"A94410","pred":"fma_id","subj":"T5618","obj":"http://purl.org/sig/ont/fma/fma7195"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T1","span":{"begin":652,"end":658},"obj":"Body_part"},{"id":"T2","span":{"begin":738,"end":742},"obj":"Body_part"},{"id":"T3","span":{"begin":1106,"end":1112},"obj":"Body_part"},{"id":"T4","span":{"begin":1140,"end":1144},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T3","span":{"begin":64,"end":97},"obj":"Disease"},{"id":"T4","span":{"begin":119,"end":127},"obj":"Disease"},{"id":"T5","span":{"begin":119,"end":123},"obj":"Disease"},{"id":"T6","span":{"begin":157,"end":165},"obj":"Disease"},{"id":"T7","span":{"begin":167,"end":175},"obj":"Disease"},{"id":"T8","span":{"begin":167,"end":171},"obj":"Disease"},{"id":"T9","span":{"begin":387,"end":395},"obj":"Disease"},{"id":"T10","span":{"begin":387,"end":391},"obj":"Disease"},{"id":"T11","span":{"begin":635,"end":643},"obj":"Disease"},{"id":"T12","span":{"begin":635,"end":639},"obj":"Disease"},{"id":"T13","span":{"begin":982,"end":998},"obj":"Disease"},{"id":"T14","span":{"begin":1022,"end":1030},"obj":"Disease"},{"id":"T15","span":{"begin":1022,"end":1026},"obj":"Disease"},{"id":"T16","span":{"begin":1145,"end":1151},"obj":"Disease"},{"id":"T17","span":{"begin":1164,"end":1173},"obj":"Disease"}],"attributes":[{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A13","pred":"mondo_id","subj":"T13","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A14","pred":"mondo_id","subj":"T14","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A15","pred":"mondo_id","subj":"T15","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A16","pred":"mondo_id","subj":"T16","obj":"http://purl.obolibrary.org/obo/MONDO_0021178"},{"id":"A17","pred":"mondo_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T96846","span":{"begin":362,"end":366},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T15043","span":{"begin":494,"end":499},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T37543","span":{"begin":505,"end":510},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T21147","span":{"begin":511,"end":518},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9443"},{"id":"T70638","span":{"begin":524,"end":529},"obj":"http://purl.obolibrary.org/obo/CLO_0007836"},{"id":"T86612","span":{"begin":537,"end":541},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T89661","span":{"begin":668,"end":672},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T73493","span":{"begin":725,"end":730},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T73667","span":{"begin":738,"end":742},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T71495","span":{"begin":738,"end":742},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T8319","span":{"begin":821,"end":826},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T72936","span":{"begin":867,"end":868},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T31033","span":{"begin":869,"end":874},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T36407","span":{"begin":897,"end":901},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T42210","span":{"begin":923,"end":929},"obj":"http://purl.obolibrary.org/obo/UBERON_0001005"},{"id":"T32994","span":{"begin":930,"end":940},"obj":"http://purl.obolibrary.org/obo/CL_0000066"},{"id":"T43681","span":{"begin":941,"end":946},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T73925","span":{"begin":1104,"end":1105},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T61785","span":{"begin":1140,"end":1144},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T98448","span":{"begin":1140,"end":1144},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T1","span":{"begin":188,"end":195},"obj":"Chemical"},{"id":"T2","span":{"begin":202,"end":213},"obj":"Chemical"},{"id":"T3","span":{"begin":304,"end":310},"obj":"Chemical"},{"id":"T4","span":{"begin":748,"end":750},"obj":"Chemical"},{"id":"T5","span":{"begin":875,"end":885},"obj":"Chemical"},{"id":"T6","span":{"begin":1064,"end":1074},"obj":"Chemical"}],"attributes":[{"id":"A1","pred":"chebi_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A2","pred":"chebi_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_48433"},{"id":"A3","pred":"chebi_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/CHEBI_17822"},{"id":"A4","pred":"chebi_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_74067"},{"id":"A5","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_52999"},{"id":"A6","pred":"chebi_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/CHEBI_52999"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T18072","span":{"begin":44,"end":56},"obj":"http://purl.obolibrary.org/obo/GO_0009405"},{"id":"T57711","span":{"begin":982,"end":998},"obj":"http://purl.obolibrary.org/obo/GO_0016032"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-sentences","denotations":[{"id":"T4","span":{"begin":0,"end":166},"obj":"Sentence"},{"id":"T5","span":{"begin":167,"end":357},"obj":"Sentence"},{"id":"T6","span":{"begin":358,"end":475},"obj":"Sentence"},{"id":"T7","span":{"begin":476,"end":681},"obj":"Sentence"},{"id":"T8","span":{"begin":682,"end":827},"obj":"Sentence"},{"id":"T9","span":{"begin":828,"end":999},"obj":"Sentence"},{"id":"T10","span":{"begin":1000,"end":1174},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}

{"project":"LitCovid-PubTator","denotations":[{"id":"35","span":{"begin":178,"end":183},"obj":"Gene"},{"id":"36","span":{"begin":185,"end":195},"obj":"Gene"},{"id":"37","span":{"begin":202,"end":233},"obj":"Gene"},{"id":"38","span":{"begin":235,"end":239},"obj":"Gene"},{"id":"39","span":{"begin":290,"end":321},"obj":"Gene"},{"id":"40","span":{"begin":323,"end":330},"obj":"Gene"},{"id":"41","span":{"begin":444,"end":448},"obj":"Gene"},{"id":"42","span":{"begin":694,"end":698},"obj":"Gene"},{"id":"43","span":{"begin":703,"end":710},"obj":"Gene"},{"id":"44","span":{"begin":859,"end":863},"obj":"Gene"},{"id":"45","span":{"begin":1064,"end":1074},"obj":"Gene"},{"id":"46","span":{"begin":1098,"end":1102},"obj":"Gene"},{"id":"47","span":{"begin":64,"end":109},"obj":"Species"},{"id":"48","span":{"begin":119,"end":129},"obj":"Species"},{"id":"49","span":{"begin":167,"end":177},"obj":"Species"},{"id":"50","span":{"begin":387,"end":397},"obj":"Species"},{"id":"51","span":{"begin":494,"end":499},"obj":"Species"},{"id":"52","span":{"begin":505,"end":510},"obj":"Species"},{"id":"53","span":{"begin":524,"end":529},"obj":"Species"},{"id":"54","span":{"begin":635,"end":645},"obj":"Species"},{"id":"55","span":{"begin":869,"end":874},"obj":"Species"},{"id":"56","span":{"begin":1022,"end":1032},"obj":"Species"},{"id":"57","span":{"begin":875,"end":885},"obj":"Gene"},{"id":"58","span":{"begin":157,"end":165},"obj":"Disease"},{"id":"59","span":{"begin":982,"end":998},"obj":"Disease"},{"id":"60","span":{"begin":1140,"end":1151},"obj":"Disease"},{"id":"61","span":{"begin":1164,"end":1173},"obj":"Disease"}],"attributes":[{"id":"A35","pred":"tao:has_database_id","subj":"35","obj":"Gene:43740568"},{"id":"A36","pred":"tao:has_database_id","subj":"36","obj":"Gene:43740568"},{"id":"A37","pred":"tao:has_database_id","subj":"37","obj":"Gene:59272"},{"id":"A38","pred":"tao:has_database_id","subj":"38","obj":"Gene:59272"},{"id":"A39","pred":"tao:has_database_id","subj":"39","obj":"Gene:7113"},{"id":"A40","pred":"tao:has_database_id","subj":"40","obj":"Gene:7113"},{"id":"A41","pred":"tao:has_database_id","subj":"41","obj":"Gene:59272"},{"id":"A42","pred":"tao:has_database_id","subj":"42","obj":"Gene:59272"},{"id":"A43","pred":"tao:has_database_id","subj":"43","obj":"Gene:7113"},{"id":"A44","pred":"tao:has_database_id","subj":"44","obj":"Gene:59272"},{"id":"A45","pred":"tao:has_database_id","subj":"45","obj":"Gene:3439"},{"id":"A46","pred":"tao:has_database_id","subj":"46","obj":"Gene:59272"},{"id":"A47","pred":"tao:has_database_id","subj":"47","obj":"Tax:694009"},{"id":"A48","pred":"tao:has_database_id","subj":"48","obj":"Tax:2697049"},{"id":"A49","pred":"tao:has_database_id","subj":"49","obj":"Tax:2697049"},{"id":"A50","pred":"tao:has_database_id","subj":"50","obj":"Tax:2697049"},{"id":"A51","pred":"tao:has_database_id","subj":"51","obj":"Tax:9606"},{"id":"A52","pred":"tao:has_database_id","subj":"52","obj":"Tax:9606"},{"id":"A53","pred":"tao:has_database_id","subj":"53","obj":"Tax:10090"},{"id":"A54","pred":"tao:has_database_id","subj":"54","obj":"Tax:2697049"},{"id":"A55","pred":"tao:has_database_id","subj":"55","obj":"Tax:9606"},{"id":"A56","pred":"tao:has_database_id","subj":"56","obj":"Tax:2697049"},{"id":"A57","pred":"tao:has_database_id","subj":"57","obj":"Gene:3439"},{"id":"A58","pred":"tao:has_database_id","subj":"58","obj":"MESH:C000657245"},{"id":"A59","pred":"tao:has_database_id","subj":"59","obj":"MESH:D001102"},{"id":"A60","pred":"tao:has_database_id","subj":"60","obj":"MESH:D055370"},{"id":"A61","pred":"tao:has_database_id","subj":"61","obj":"MESH:D007239"}],"namespaces":[{"prefix":"Tax","uri":"https://www.ncbi.nlm.nih.gov/taxonomy/"},{"prefix":"MESH","uri":"https://id.nlm.nih.gov/mesh/"},{"prefix":"Gene","uri":"https://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"CVCL","uri":"https://web.expasy.org/cellosaurus/CVCL_"}],"text":"There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2), which causes the disease COVID-19. SARS-CoV-2 spike (S) protein binds angiotensin-converting enzyme 2 (ACE2), and in concert with host proteases, principally transmembrane serine protease 2 (TMPRSS2), promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues and the factors that regulate ACE2 expression remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 among tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discovered that ACE2 is a human interferon-stimulated gene (ISG) in vitro using airway epithelial cells and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection."}