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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T12","span":{"begin":709,"end":726},"obj":"Body_part"},{"id":"T13","span":{"begin":756,"end":760},"obj":"Body_part"},{"id":"T14","span":{"begin":852,"end":857},"obj":"Body_part"}],"attributes":[{"id":"A12","pred":"fma_id","subj":"T12","obj":"http://purl.org/sig/ont/fma/fma9640"},{"id":"A13","pred":"fma_id","subj":"T13","obj":"http://purl.org/sig/ont/fma/fma7195"},{"id":"A14","pred":"fma_id","subj":"T14","obj":"http://purl.org/sig/ont/fma/fma67498"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T4","span":{"begin":709,"end":726},"obj":"Body_part"},{"id":"T5","span":{"begin":720,"end":726},"obj":"Body_part"},{"id":"T6","span":{"begin":756,"end":760},"obj":"Body_part"},{"id":"T7","span":{"begin":852,"end":857},"obj":"Body_part"}],"attributes":[{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/UBERON_0002384"},{"id":"A5","pred":"uberon_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T37","span":{"begin":3,"end":6},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T38","span":{"begin":190,"end":191},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T39","span":{"begin":233,"end":234},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T40","span":{"begin":471,"end":472},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T41","span":{"begin":482,"end":484},"obj":"http://purl.obolibrary.org/obo/CLO_0050507"},{"id":"T42","span":{"begin":709,"end":726},"obj":"http://purl.obolibrary.org/obo/UBERON_0002384"},{"id":"T43","span":{"begin":709,"end":726},"obj":"http://www.ebi.ac.uk/efo/EFO_0000952"},{"id":"T44","span":{"begin":756,"end":760},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T45","span":{"begin":756,"end":760},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T46","span":{"begin":842,"end":843},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T47","span":{"begin":852,"end":857},"obj":"http://purl.obolibrary.org/obo/UBERON_0003103"},{"id":"T48","span":{"begin":905,"end":907},"obj":"http://purl.obolibrary.org/obo/CLO_0050509"},{"id":"T49","span":{"begin":913,"end":914},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T50","span":{"begin":1024,"end":1025},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T5","span":{"begin":473,"end":478},"obj":"Chemical"}],"attributes":[{"id":"A5","pred":"chebi_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/CHEBI_24433"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T29","span":{"begin":326,"end":335},"obj":"Phenotype"},{"id":"T30","span":{"begin":519,"end":531},"obj":"Phenotype"},{"id":"T31","span":{"begin":558,"end":577},"obj":"Phenotype"},{"id":"T32","span":{"begin":743,"end":768},"obj":"Phenotype"},{"id":"T33","span":{"begin":867,"end":879},"obj":"Phenotype"},{"id":"T34","span":{"begin":994,"end":1003},"obj":"Phenotype"},{"id":"T35","span":{"begin":1062,"end":1080},"obj":"Phenotype"}],"attributes":[{"id":"A29","pred":"hp_id","subj":"T29","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A30","pred":"hp_id","subj":"T30","obj":"http://purl.obolibrary.org/obo/HP_0002960"},{"id":"A31","pred":"hp_id","subj":"T31","obj":"http://purl.obolibrary.org/obo/HP_0002878"},{"id":"A32","pred":"hp_id","subj":"T32","obj":"http://purl.obolibrary.org/obo/HP_0006530"},{"id":"A33","pred":"hp_id","subj":"T33","obj":"http://purl.obolibrary.org/obo/HP_0002960"},{"id":"A34","pred":"hp_id","subj":"T34","obj":"http://purl.obolibrary.org/obo/HP_0002090"},{"id":"A35","pred":"hp_id","subj":"T35","obj":"http://purl.obolibrary.org/obo/HP_0002960"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T18","span":{"begin":0,"end":377},"obj":"Sentence"},{"id":"T19","span":{"begin":378,"end":578},"obj":"Sentence"},{"id":"T20","span":{"begin":579,"end":909},"obj":"Sentence"},{"id":"T21","span":{"begin":910,"end":1181},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PMC-OGER-BB

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T69","span":{"begin":140,"end":148},"obj":"SP_7"},{"id":"T70","span":{"begin":166,"end":176},"obj":"SP_7"},{"id":"T71","span":{"begin":241,"end":251},"obj":"UBERON:0002405"},{"id":"T72","span":{"begin":276,"end":289},"obj":"GO:0065007"},{"id":"T73","span":{"begin":313,"end":325},"obj":"UBERON:0005169"},{"id":"T74","span":{"begin":340,"end":347},"obj":"SO:0000704"},{"id":"T75","span":{"begin":360,"end":371},"obj":"NCBITaxon:1"},{"id":"T76","span":{"begin":535,"end":545},"obj":"SP_7"},{"id":"T77","span":{"begin":558,"end":569},"obj":"UBERON:0001004"},{"id":"T78","span":{"begin":658,"end":666},"obj":"SP_7"},{"id":"T79","span":{"begin":709,"end":726},"obj":"UBERON:0002384"},{"id":"T80","span":{"begin":743,"end":755},"obj":"UBERON:0005169"},{"id":"T81","span":{"begin":756,"end":760},"obj":"UBERON:0002048"},{"id":"T82","span":{"begin":795,"end":805},"obj":"SP_7"},{"id":"T83","span":{"begin":852,"end":857},"obj":"UBERON:0000062"},{"id":"T84","span":{"begin":983,"end":993},"obj":"SP_7"},{"id":"T85","span":{"begin":1062,"end":1072},"obj":"UBERON:0002405"},{"id":"T86","span":{"begin":1089,"end":1103},"obj":"GO:0042571"},{"id":"T87","span":{"begin":1167,"end":1175},"obj":"SP_7"},{"id":"T15503","span":{"begin":140,"end":148},"obj":"SP_7"},{"id":"T24030","span":{"begin":166,"end":176},"obj":"SP_7"},{"id":"T85118","span":{"begin":241,"end":251},"obj":"UBERON:0002405"},{"id":"T75819","span":{"begin":276,"end":289},"obj":"GO:0065007"},{"id":"T41445","span":{"begin":313,"end":325},"obj":"UBERON:0005169"},{"id":"T67454","span":{"begin":340,"end":347},"obj":"SO:0000704"},{"id":"T9657","span":{"begin":360,"end":371},"obj":"NCBITaxon:1"},{"id":"T48049","span":{"begin":535,"end":545},"obj":"SP_7"},{"id":"T36327","span":{"begin":558,"end":569},"obj":"UBERON:0001004"},{"id":"T49541","span":{"begin":658,"end":666},"obj":"SP_7"},{"id":"T55349","span":{"begin":709,"end":726},"obj":"UBERON:0002384"},{"id":"T28114","span":{"begin":743,"end":755},"obj":"UBERON:0005169"},{"id":"T77496","span":{"begin":756,"end":760},"obj":"UBERON:0002048"},{"id":"T55588","span":{"begin":795,"end":805},"obj":"SP_7"},{"id":"T72508","span":{"begin":852,"end":857},"obj":"UBERON:0000062"},{"id":"T73018","span":{"begin":983,"end":993},"obj":"SP_7"},{"id":"T73200","span":{"begin":1062,"end":1072},"obj":"UBERON:0002405"},{"id":"T76547","span":{"begin":1089,"end":1103},"obj":"GO:0042571"},{"id":"T88308","span":{"begin":1167,"end":1175},"obj":"SP_7"}],"text":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

LitCovid-PubTator

{"project":"LitCovid-PubTator","denotations":[{"id":"128","span":{"begin":166,"end":176},"obj":"Species"},{"id":"129","span":{"begin":485,"end":493},"obj":"Species"},{"id":"130","span":{"begin":535,"end":545},"obj":"Species"},{"id":"131","span":{"begin":895,"end":903},"obj":"Species"},{"id":"132","span":{"begin":960,"end":968},"obj":"Species"},{"id":"133","span":{"begin":108,"end":135},"obj":"Disease"},{"id":"134","span":{"begin":140,"end":148},"obj":"Disease"},{"id":"135","span":{"begin":326,"end":335},"obj":"Disease"},{"id":"136","span":{"begin":558,"end":577},"obj":"Disease"},{"id":"137","span":{"begin":658,"end":666},"obj":"Disease"},{"id":"138","span":{"begin":678,"end":682},"obj":"Disease"},{"id":"139","span":{"begin":743,"end":768},"obj":"Disease"},{"id":"140","span":{"begin":795,"end":815},"obj":"Disease"},{"id":"141","span":{"begin":983,"end":1003},"obj":"Disease"},{"id":"142","span":{"begin":1062,"end":1080},"obj":"Disease"},{"id":"143","span":{"begin":1167,"end":1175},"obj":"Disease"}],"attributes":[{"id":"A128","pred":"tao:has_database_id","subj":"128","obj":"Tax:2697049"},{"id":"A129","pred":"tao:has_database_id","subj":"129","obj":"Tax:9606"},{"id":"A130","pred":"tao:has_database_id","subj":"130","obj":"Tax:2697049"},{"id":"A131","pred":"tao:has_database_id","subj":"131","obj":"Tax:9606"},{"id":"A132","pred":"tao:has_database_id","subj":"132","obj":"Tax:9606"},{"id":"A133","pred":"tao:has_database_id","subj":"133","obj":"MESH:D007249"},{"id":"A134","pred":"tao:has_database_id","subj":"134","obj":"MESH:C000657245"},{"id":"A135","pred":"tao:has_database_id","subj":"135","obj":"MESH:D011014"},{"id":"A136","pred":"tao:has_database_id","subj":"136","obj":"MESH:D012131"},{"id":"A137","pred":"tao:has_database_id","subj":"137","obj":"MESH:C000657245"},{"id":"A138","pred":"tao:has_database_id","subj":"138","obj":"MESH:D012128"},{"id":"A139","pred":"tao:has_database_id","subj":"139","obj":"MESH:D017563"},{"id":"A140","pred":"tao:has_database_id","subj":"140","obj":"MESH:C000657245"},{"id":"A141","pred":"tao:has_database_id","subj":"141","obj":"MESH:C000657245"},{"id":"A142","pred":"tao:has_database_id","subj":"142","obj":"MESH:D001327"},{"id":"A143","pred":"tao:has_database_id","subj":"143","obj":"MESH:C000657245"}],"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":"It has been suggested that the shared pathogenetic mechanisms and clinical-radiological aspects between the hyper-inflammatory diseases and Covid-19 may suggest that SARS-CoV-2 could act as a triggering factor for the development of a rapid autoimmune and/or autoinflammatory dysregulation, leading to the severe interstitial pneumonia, in genetic predisposed individuals [26]. Furthermore, in an online pre-published study from Germany the authors studied prospectively a group of 22 patients for the possible role of autoimmunity in SARS-CoV-2 -associated respiratory failure. Based on serological, radiological and histomorphological similarities between Covid-19-associated ARDS and acute exacerbation of connective tissue disease induced interstitial lung disease, the authors suggest that SARS-CoV-2 infection might trigger or simulate a form of organ specific autoimmunity in predisposed patients [27]. In a similar retrospective study from China of 21 patients with critical SARS-CoV-2 pneumonia, the authors showed a prevalence of between 20 and 50% of autoimmune disease related autoantibodies, suggesting the rational for immunosupression in such cases of Covid-19 [28]."}

PMC:7289100 / 3480-4661 JSONTXT

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PMC:7289100 / 3480-4661 JSON TXT