PMC:7346000 / 9471-10723 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T31","span":{"begin":12,"end":16},"obj":"Body_part"},{"id":"T32","span":{"begin":238,"end":247},"obj":"Body_part"},{"id":"T33","span":{"begin":429,"end":433},"obj":"Body_part"},{"id":"T34","span":{"begin":454,"end":467},"obj":"Body_part"},{"id":"T35","span":{"begin":644,"end":654},"obj":"Body_part"}],"attributes":[{"id":"A31","pred":"fma_id","subj":"T31","obj":"http://purl.org/sig/ont/fma/fma256135"},{"id":"A32","pred":"fma_id","subj":"T32","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A33","pred":"fma_id","subj":"T33","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A34","pred":"fma_id","subj":"T34","obj":"http://purl.org/sig/ont/fma/fma62870"},{"id":"A35","pred":"fma_id","subj":"T35","obj":"http://purl.org/sig/ont/fma/fma62863"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-PubTator","denotations":[{"id":"309","span":{"begin":257,"end":260},"obj":"Gene"},{"id":"310","span":{"begin":95,"end":103},"obj":"Species"},{"id":"311","span":{"begin":279,"end":287},"obj":"Species"},{"id":"312","span":{"begin":524,"end":532},"obj":"Species"},{"id":"313","span":{"begin":851,"end":859},"obj":"Species"},{"id":"314","span":{"begin":1014,"end":1024},"obj":"Species"},{"id":"315","span":{"begin":116,"end":136},"obj":"Disease"},{"id":"316","span":{"begin":344,"end":354},"obj":"Disease"},{"id":"317","span":{"begin":538,"end":546},"obj":"Disease"},{"id":"318","span":{"begin":732,"end":747},"obj":"Disease"},{"id":"319","span":{"begin":826,"end":847},"obj":"Disease"},{"id":"320","span":{"begin":1141,"end":1145},"obj":"Disease"},{"id":"321","span":{"begin":1217,"end":1237},"obj":"Disease"}],"attributes":[{"id":"A309","pred":"tao:has_database_id","subj":"309","obj":"Gene:7124"},{"id":"A310","pred":"tao:has_database_id","subj":"310","obj":"Tax:9606"},{"id":"A311","pred":"tao:has_database_id","subj":"311","obj":"Tax:9606"},{"id":"A312","pred":"tao:has_database_id","subj":"312","obj":"Tax:9606"},{"id":"A313","pred":"tao:has_database_id","subj":"313","obj":"Tax:9606"},{"id":"A314","pred":"tao:has_database_id","subj":"314","obj":"Tax:2697049"},{"id":"A315","pred":"tao:has_database_id","subj":"315","obj":"MESH:C000657245"},{"id":"A316","pred":"tao:has_database_id","subj":"316","obj":"MESH:D007239"},{"id":"A317","pred":"tao:has_database_id","subj":"317","obj":"MESH:C000657245"},{"id":"A318","pred":"tao:has_database_id","subj":"318","obj":"MESH:D008231"},{"id":"A319","pred":"tao:has_database_id","subj":"319","obj":"MESH:D009361"},{"id":"A320","pred":"tao:has_database_id","subj":"320","obj":"MESH:D012128"},{"id":"A321","pred":"tao:has_database_id","subj":"321","obj":"MESH:D060085"}],"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":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T104","span":{"begin":116,"end":124},"obj":"Disease"},{"id":"T105","span":{"begin":127,"end":136},"obj":"Disease"},{"id":"T106","span":{"begin":168,"end":172},"obj":"Disease"},{"id":"T107","span":{"begin":344,"end":354},"obj":"Disease"},{"id":"T108","span":{"begin":502,"end":520},"obj":"Disease"},{"id":"T109","span":{"begin":538,"end":546},"obj":"Disease"},{"id":"T110","span":{"begin":732,"end":747},"obj":"Disease"},{"id":"T111","span":{"begin":1014,"end":1022},"obj":"Disease"},{"id":"T112","span":{"begin":1141,"end":1145},"obj":"Disease"},{"id":"T113","span":{"begin":1227,"end":1237},"obj":"Disease"},{"id":"T114","span":{"begin":1247,"end":1251},"obj":"Disease"}],"attributes":[{"id":"A104","pred":"mondo_id","subj":"T104","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A105","pred":"mondo_id","subj":"T105","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A106","pred":"mondo_id","subj":"T106","obj":"http://purl.obolibrary.org/obo/MONDO_0007163"},{"id":"A107","pred":"mondo_id","subj":"T107","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A108","pred":"mondo_id","subj":"T108","obj":"http://purl.obolibrary.org/obo/MONDO_0005046"},{"id":"A109","pred":"mondo_id","subj":"T109","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"},{"id":"A110","pred":"mondo_id","subj":"T110","obj":"http://purl.obolibrary.org/obo/MONDO_0003783"},{"id":"A111","pred":"mondo_id","subj":"T111","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A112","pred":"mondo_id","subj":"T112","obj":"http://purl.obolibrary.org/obo/MONDO_0006502"},{"id":"A113","pred":"mondo_id","subj":"T113","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A114","pred":"mondo_id","subj":"T114","obj":"http://purl.obolibrary.org/obo/MONDO_0007163"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T75","span":{"begin":356,"end":358},"obj":"http://purl.obolibrary.org/obo/CLO_0001000"},{"id":"T76","span":{"begin":429,"end":433},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T77","span":{"begin":548,"end":550},"obj":"http://purl.obolibrary.org/obo/CLO_0001313"},{"id":"T78","span":{"begin":773,"end":774},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T23","span":{"begin":588,"end":601},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T24","span":{"begin":994,"end":1010},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T25","span":{"begin":1048,"end":1065},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T26","span":{"begin":1048,"end":1065},"obj":"http://purl.obolibrary.org/obo/GO_0019058"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-PD-HP","denotations":[{"id":"T17","span":{"begin":109,"end":136},"obj":"Phenotype"},{"id":"T18","span":{"begin":732,"end":747},"obj":"Phenotype"}],"attributes":[{"id":"A17","pred":"hp_id","subj":"T17","obj":"http://purl.obolibrary.org/obo/HP_0033141"},{"id":"A18","pred":"hp_id","subj":"T18","obj":"http://purl.obolibrary.org/obo/HP_0001888"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"LitCovid-sentences","denotations":[{"id":"T52","span":{"begin":0,"end":173},"obj":"Sentence"},{"id":"T53","span":{"begin":174,"end":360},"obj":"Sentence"},{"id":"T54","span":{"begin":361,"end":552},"obj":"Sentence"},{"id":"T55","span":{"begin":553,"end":708},"obj":"Sentence"},{"id":"T56","span":{"begin":709,"end":896},"obj":"Sentence"},{"id":"T57","span":{"begin":897,"end":1252},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}

{"project":"2_test","denotations":[{"id":"32599813-31986264-60095088","span":{"begin":356,"end":358},"obj":"31986264"},{"id":"32599813-32161940-60095089","span":{"begin":548,"end":550},"obj":"32161940"},{"id":"32599813-32320677-60095090","span":{"begin":639,"end":641},"obj":"32320677"},{"id":"32599813-30974130-60095091","span":{"begin":892,"end":894},"obj":"30974130"},{"id":"32599813-32437659-60095092","span":{"begin":1147,"end":1149},"obj":"32437659"}],"text":"An emerging body of evidence supports therefore an increased systemic inflammatory reaction in patients with severe SARS-CoV-2 infection who are more likely to develop CAPA. In this regard, increased levels of circulating proinflammatory cytokines, such as TNF, were observed in patients requiring intensive care, compared to those with milder infections [35]. Other studies, however, have also unveiled marked defects in immune cell populations, namely T-lymphocytes, as another factor explaining the immune dysfunction in patients with COVID-19 [36]. This suggests that while sustained innate immune function leads to hyperinflammation [37], lymphocyte numbers decline, and their function may be defective. In this regard, severe lymphocytopenia was among the factors in a risk score model that predicted the development of invasive mold disease in patients with hematological malignances [38]. It is thus reasonable to speculate that in elderly individuals or with co-morbidities, defective immune responses to SARS-CoV-2 may allow unrestricted viral replication which, in turn, elicits hyperinflammation and severe complications such as ARDS [39], besides establishing favorable conditions for the acquisition of secondary infections, such as CAPA."}