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LitCovid-PD-FMA-UBERON

LitCovid-PD-UBERON

{"project":"LitCovid-PD-UBERON","denotations":[{"id":"T159","span":{"begin":775,"end":779},"obj":"Body_part"},{"id":"T160","span":{"begin":1129,"end":1133},"obj":"Body_part"},{"id":"T161","span":{"begin":1228,"end":1233},"obj":"Body_part"}],"attributes":[{"id":"A159","pred":"uberon_id","subj":"T159","obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"A160","pred":"uberon_id","subj":"T160","obj":"http://purl.obolibrary.org/obo/UBERON_0002398"},{"id":"A161","pred":"uberon_id","subj":"T161","obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]."}

LitCovid-PubTator

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T994","span":{"begin":129,"end":135},"obj":"http://purl.obolibrary.org/obo/UBERON_0001969"},{"id":"T995","span":{"begin":222,"end":225},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T996","span":{"begin":243,"end":244},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T997","span":{"begin":353,"end":356},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T998","span":{"begin":598,"end":606},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_9443"},{"id":"T999","span":{"begin":639,"end":640},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T1000","span":{"begin":689,"end":696},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_33208"},{"id":"T1001","span":{"begin":752,"end":753},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T1002","span":{"begin":775,"end":779},"obj":"http://purl.obolibrary.org/obo/UBERON_0002048"},{"id":"T1003","span":{"begin":775,"end":779},"obj":"http://www.ebi.ac.uk/efo/EFO_0000934"},{"id":"T1004","span":{"begin":859,"end":860},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T1005","span":{"begin":1026,"end":1034},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T1006","span":{"begin":1188,"end":1189},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T1007","span":{"begin":1344,"end":1349},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T1008","span":{"begin":1359,"end":1362},"obj":"http://purl.obolibrary.org/obo/PR_000001004"},{"id":"T1009","span":{"begin":1363,"end":1370},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T1010","span":{"begin":1789,"end":1799},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T1011","span":{"begin":2070,"end":2071},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]."}

LitCovid-PD-CHEBI

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T405","span":{"begin":0,"end":107},"obj":"Sentence"},{"id":"T406","span":{"begin":108,"end":503},"obj":"Sentence"},{"id":"T407","span":{"begin":504,"end":680},"obj":"Sentence"},{"id":"T408","span":{"begin":681,"end":931},"obj":"Sentence"},{"id":"T409","span":{"begin":932,"end":1115},"obj":"Sentence"},{"id":"T410","span":{"begin":1116,"end":1427},"obj":"Sentence"},{"id":"T411","span":{"begin":1428,"end":1842},"obj":"Sentence"},{"id":"T412","span":{"begin":1843,"end":2039},"obj":"Sentence"},{"id":"T413","span":{"begin":2040,"end":2159},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T142","span":{"begin":762,"end":768},"obj":"Phenotype"},{"id":"T143","span":{"begin":1087,"end":1093},"obj":"Phenotype"},{"id":"T144","span":{"begin":1190,"end":1204},"obj":"Phenotype"},{"id":"T145","span":{"begin":1491,"end":1502},"obj":"Phenotype"},{"id":"T146","span":{"begin":1510,"end":1521},"obj":"Phenotype"},{"id":"T147","span":{"begin":1545,"end":1552},"obj":"Phenotype"},{"id":"T148","span":{"begin":1658,"end":1665},"obj":"Phenotype"}],"attributes":[{"id":"A142","pred":"hp_id","subj":"T142","obj":"http://purl.obolibrary.org/obo/HP_0002099"},{"id":"A143","pred":"hp_id","subj":"T143","obj":"http://purl.obolibrary.org/obo/HP_0002099"},{"id":"A144","pred":"hp_id","subj":"T144","obj":"http://purl.obolibrary.org/obo/HP_0033041"},{"id":"A145","pred":"hp_id","subj":"T145","obj":"http://purl.obolibrary.org/obo/HP_0001649"},{"id":"A146","pred":"hp_id","subj":"T146","obj":"http://purl.obolibrary.org/obo/HP_0002615"},{"id":"A147","pred":"hp_id","subj":"T147","obj":"http://purl.obolibrary.org/obo/HP_0012418"},{"id":"A148","pred":"hp_id","subj":"T148","obj":"http://purl.obolibrary.org/obo/HP_0012418"}],"text":"There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]."}

2_test

{"project":"2_test","denotations":[{"id":"32708755-32065055-20678966","span":{"begin":313,"end":315},"obj":"32065055"},{"id":"32708755-32366817-20678967","span":{"begin":316,"end":318},"obj":"32366817"},{"id":"32708755-32404477-20678968","span":{"begin":319,"end":321},"obj":"32404477"},{"id":"32708755-32253318-20678969","span":{"begin":325,"end":327},"obj":"32253318"},{"id":"32708755-32243945-20678970","span":{"begin":328,"end":330},"obj":"32243945"},{"id":"32708755-32505227-20678971","span":{"begin":331,"end":334},"obj":"32505227"},{"id":"32708755-21937658-20678972","span":{"begin":926,"end":929},"obj":"21937658"},{"id":"32708755-18832706-20678973","span":{"begin":1422,"end":1425},"obj":"18832706"},{"id":"32708755-32171076-20678974","span":{"begin":2156,"end":2157},"obj":"32171076"}],"text":"There is currently no specific pharmacotherapy to combat SARS-CoV-2 infection and its pathological effects. Actually, the use of plasma from convalescent COVID-19 patients or of SARS-CoV-2-specific neutralizing antibodies has been shown to be a promising option for the treatment of critically COVID-19 patients [32,33,34,35,36,37,172,173]; however, it has some limitations that might be overcome by vaccine strategies or by the production of specific anti SARS-Co-V-2 therapeutic monoclonal antibodies. Despite the promising data that demonstrate vaccine protection against SARS-CoV-2 in nonhuman primates [174], we cannot be sure to get a vaccine against SARS-CoV-2 (see [175]). Indeed, animals immunized with inactivated SARS-CoV vaccines developed a severe (asthma-like) lung eosinophilic immunopathology when challenged with SARS-CoV, further indicating a central role of eosinophil “balanced numbers” in this pathology [176]. Vaccines might generate antibodies against viral ligand/ACE2 complex that finally blocks ACE2 activity during SARS-CoV infection and consequent downstream asthma-like events/symptoms. On the other hand, fatal outcomes in SARS-CoV infection correlated with a cytokine storm involving elevated Th2 serum cytokines (including IL-4, IL-5 and IL-10), suggesting that an increase of Th2 cytokines possibly mediated by virus-specific CD4 T cells might be crucial in the severe forms of infection [110]. In addition to cytokine profile (such as IL-10), eosinopaenia, tachycardia, normo/hypotension (although COVID-19 and hypoxia increase Ang II and many patients are “hypertensive” and/or receiving anti-hypertensive medications) and hypoxia in SARS-CoV-2 patients are compatible with downstream events stemming from both an excessive ACE2 pathway upregulation and activation of positive feedback loops (see Figure 2). ACE2 and (anti-inflammatory) IL-10 hyperproduction may ultimately trigger subsequent compensatory (and deleterious) responses, leading to both renin/ACE and pro-inflammatory cytokine upregulation. In line with this hypothesis, a longitudinal study showed that IL-6 increases late during the COVID-19 progression [3]."}

PMC:7408073 / 82419-84578 JSONTXT

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PMC:7408073 / 82419-84578 JSON TXT