PMC:7252096 / 65151-66544 JSON TXT

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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T825","span":{"begin":207,"end":223},"obj":"Body_part"},{"id":"T826","span":{"begin":218,"end":223},"obj":"Body_part"},{"id":"T827","span":{"begin":661,"end":665},"obj":"Body_part"},{"id":"T828","span":{"begin":1213,"end":1217},"obj":"Body_part"}],"attributes":[{"id":"A825","pred":"fma_id","subj":"T825","obj":"http://purl.org/sig/ont/fma/fma66768"},{"id":"A826","pred":"fma_id","subj":"T826","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A827","pred":"fma_id","subj":"T827","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A828","pred":"fma_id","subj":"T828","obj":"http://purl.org/sig/ont/fma/fma68646"}],"text":"As SARS-CoV-S leads to ACE2-receptor-mediated internalization, the host IFN response could thus promote the ability for SARS-CoV and SARS-CoV-2 to maintain cellular targets in neighboring human upper airway epithelial cells. Altogether along with a study of HCoV-OC43, which co-opts IFN-inducible transmembrane 2 (IFITM2) and IFITM3 to promote viral entry, this adds to the growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN pathway (Fung and Liu, 2019, Mar et al., 2018, Zhao et al., 2014). Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016, Channappanavar et al., 2019, Channappanavar and Perlman, 2017, Davidson et al., 2015); and other factors such as co-infection, age, gender, and co-morbidities, among others. Understanding the specific host restriction factors targeting SARS-CoV-2 and identifying specific drivers of these genes in the absence of ACE2 upregulation might provide strategies to dissociate the dual roles of IFN in certain coronavirus infections. Whether IFNs upregulate ACE2 in putative target cell subsets in vivo will be of significant interest to define in future work once current COVID-19-related restrictions on basic scientific inquiry are lifted (Qian et al., 2013)."}

LitCovid-PD-MONDO

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T241","span":{"begin":3,"end":11},"obj":"Disease"},{"id":"T242","span":{"begin":3,"end":7},"obj":"Disease"},{"id":"T243","span":{"begin":120,"end":128},"obj":"Disease"},{"id":"T244","span":{"begin":120,"end":124},"obj":"Disease"},{"id":"T245","span":{"begin":133,"end":141},"obj":"Disease"},{"id":"T246","span":{"begin":133,"end":137},"obj":"Disease"},{"id":"T247","span":{"begin":650,"end":659},"obj":"Disease"},{"id":"T248","span":{"begin":691,"end":695},"obj":"Disease"},{"id":"T249","span":{"begin":854,"end":863},"obj":"Disease"},{"id":"T250","span":{"begin":974,"end":982},"obj":"Disease"},{"id":"T251","span":{"begin":974,"end":978},"obj":"Disease"},{"id":"T252","span":{"begin":1153,"end":1163},"obj":"Disease"},{"id":"T253","span":{"begin":1304,"end":1312},"obj":"Disease"}],"attributes":[{"id":"A241","pred":"mondo_id","subj":"T241","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A242","pred":"mondo_id","subj":"T242","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A243","pred":"mondo_id","subj":"T243","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A244","pred":"mondo_id","subj":"T244","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A245","pred":"mondo_id","subj":"T245","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A246","pred":"mondo_id","subj":"T246","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A247","pred":"mondo_id","subj":"T247","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A248","pred":"mondo_id","subj":"T248","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A249","pred":"mondo_id","subj":"T249","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A250","pred":"mondo_id","subj":"T250","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A251","pred":"mondo_id","subj":"T251","obj":"http://purl.obolibrary.org/obo/MONDO_0005091"},{"id":"A252","pred":"mondo_id","subj":"T252","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A253","pred":"mondo_id","subj":"T253","obj":"http://purl.obolibrary.org/obo/MONDO_0100096"}],"text":"As SARS-CoV-S leads to ACE2-receptor-mediated internalization, the host IFN response could thus promote the ability for SARS-CoV and SARS-CoV-2 to maintain cellular targets in neighboring human upper airway epithelial cells. Altogether along with a study of HCoV-OC43, which co-opts IFN-inducible transmembrane 2 (IFITM2) and IFITM3 to promote viral entry, this adds to the growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN pathway (Fung and Liu, 2019, Mar et al., 2018, Zhao et al., 2014). Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016, Channappanavar et al., 2019, Channappanavar and Perlman, 2017, Davidson et al., 2015); and other factors such as co-infection, age, gender, and co-morbidities, among others. Understanding the specific host restriction factors targeting SARS-CoV-2 and identifying specific drivers of these genes in the absence of ACE2 upregulation might provide strategies to dissociate the dual roles of IFN in certain coronavirus infections. Whether IFNs upregulate ACE2 in putative target cell subsets in vivo will be of significant interest to define in future work once current COVID-19-related restrictions on basic scientific inquiry are lifted (Qian et al., 2013)."}

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T1186","span":{"begin":188,"end":193},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T1187","span":{"begin":200,"end":206},"obj":"http://purl.obolibrary.org/obo/UBERON_0001005"},{"id":"T1188","span":{"begin":207,"end":217},"obj":"http://purl.obolibrary.org/obo/CL_0000066"},{"id":"T1189","span":{"begin":218,"end":223},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1190","span":{"begin":247,"end":248},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T1191","span":{"begin":428,"end":435},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T1192","span":{"begin":478,"end":483},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9606"},{"id":"T1193","span":{"begin":529,"end":533},"obj":"http://purl.obolibrary.org/obo/CLO_0001185"},{"id":"T1194","span":{"begin":661,"end":665},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T1195","span":{"begin":1027,"end":1032},"obj":"http://purl.obolibrary.org/obo/OGG_0000000002"},{"id":"T1196","span":{"begin":1213,"end":1217},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"As SARS-CoV-S leads to ACE2-receptor-mediated internalization, the host IFN response could thus promote the ability for SARS-CoV and SARS-CoV-2 to maintain cellular targets in neighboring human upper airway epithelial cells. Altogether along with a study of HCoV-OC43, which co-opts IFN-inducible transmembrane 2 (IFITM2) and IFITM3 to promote viral entry, this adds to the growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN pathway (Fung and Liu, 2019, Mar et al., 2018, Zhao et al., 2014). Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016, Channappanavar et al., 2019, Channappanavar and Perlman, 2017, Davidson et al., 2015); and other factors such as co-infection, age, gender, and co-morbidities, among others. Understanding the specific host restriction factors targeting SARS-CoV-2 and identifying specific drivers of these genes in the absence of ACE2 upregulation might provide strategies to dissociate the dual roles of IFN in certain coronavirus infections. Whether IFNs upregulate ACE2 in putative target cell subsets in vivo will be of significant interest to define in future work once current COVID-19-related restrictions on basic scientific inquiry are lifted (Qian et al., 2013)."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T427","span":{"begin":0,"end":224},"obj":"Sentence"},{"id":"T428","span":{"begin":225,"end":554},"obj":"Sentence"},{"id":"T429","span":{"begin":555,"end":911},"obj":"Sentence"},{"id":"T430","span":{"begin":912,"end":1164},"obj":"Sentence"},{"id":"T431","span":{"begin":1165,"end":1393},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"As SARS-CoV-S leads to ACE2-receptor-mediated internalization, the host IFN response could thus promote the ability for SARS-CoV and SARS-CoV-2 to maintain cellular targets in neighboring human upper airway epithelial cells. Altogether along with a study of HCoV-OC43, which co-opts IFN-inducible transmembrane 2 (IFITM2) and IFITM3 to promote viral entry, this adds to the growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN pathway (Fung and Liu, 2019, Mar et al., 2018, Zhao et al., 2014). Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016, Channappanavar et al., 2019, Channappanavar and Perlman, 2017, Davidson et al., 2015); and other factors such as co-infection, age, gender, and co-morbidities, among others. Understanding the specific host restriction factors targeting SARS-CoV-2 and identifying specific drivers of these genes in the absence of ACE2 upregulation might provide strategies to dissociate the dual roles of IFN in certain coronavirus infections. Whether IFNs upregulate ACE2 in putative target cell subsets in vivo will be of significant interest to define in future work once current COVID-19-related restrictions on basic scientific inquiry are lifted (Qian et al., 2013)."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"32413319-31226023-20790525","span":{"begin":511,"end":515},"obj":"31226023"},{"id":"32413319-30190477-20790526","span":{"begin":529,"end":533},"obj":"30190477"},{"id":"32413319-24753610-20790527","span":{"begin":548,"end":552},"obj":"24753610"},{"id":"32413319-26867177-20790528","span":{"begin":732,"end":736},"obj":"26867177"},{"id":"32413319-31355779-20790529","span":{"begin":761,"end":765},"obj":"31355779"},{"id":"32413319-28466096-20790530","span":{"begin":795,"end":799},"obj":"28466096"},{"id":"32413319-25714109-20790531","span":{"begin":818,"end":822},"obj":"25714109"},{"id":"32413319-23418343-20790532","span":{"begin":1387,"end":1391},"obj":"23418343"}],"text":"As SARS-CoV-S leads to ACE2-receptor-mediated internalization, the host IFN response could thus promote the ability for SARS-CoV and SARS-CoV-2 to maintain cellular targets in neighboring human upper airway epithelial cells. Altogether along with a study of HCoV-OC43, which co-opts IFN-inducible transmembrane 2 (IFITM2) and IFITM3 to promote viral entry, this adds to the growing evidence that coronaviruses, as well as other viruses, have evolved to leverage features of the human IFN pathway (Fung and Liu, 2019, Mar et al., 2018, Zhao et al., 2014). Whether type I IFNs are net protective or detrimental to the host might depend on the stage of infection; cell subsets in question; the SARS viral clade (Channappanavar et al., 2016, Channappanavar et al., 2019, Channappanavar and Perlman, 2017, Davidson et al., 2015); and other factors such as co-infection, age, gender, and co-morbidities, among others. Understanding the specific host restriction factors targeting SARS-CoV-2 and identifying specific drivers of these genes in the absence of ACE2 upregulation might provide strategies to dissociate the dual roles of IFN in certain coronavirus infections. Whether IFNs upregulate ACE2 in putative target cell subsets in vivo will be of significant interest to define in future work once current COVID-19-related restrictions on basic scientific inquiry are lifted (Qian et al., 2013)."}