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LitCovid-PD-FMA-UBERON

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T85","span":{"begin":622,"end":625},"obj":"Body_part"},{"id":"T86","span":{"begin":640,"end":643},"obj":"Body_part"},{"id":"T87","span":{"begin":711,"end":716},"obj":"Body_part"},{"id":"T88","span":{"begin":871,"end":875},"obj":"Body_part"},{"id":"T89","span":{"begin":962,"end":971},"obj":"Body_part"},{"id":"T90","span":{"begin":976,"end":980},"obj":"Body_part"},{"id":"T91","span":{"begin":1013,"end":1021},"obj":"Body_part"},{"id":"T92","span":{"begin":1045,"end":1049},"obj":"Body_part"},{"id":"T93","span":{"begin":1208,"end":1216},"obj":"Body_part"},{"id":"T94","span":{"begin":1301,"end":1309},"obj":"Body_part"}],"attributes":[{"id":"A85","pred":"fma_id","subj":"T85","obj":"http://purl.org/sig/ont/fma/fma62872"},{"id":"A86","pred":"fma_id","subj":"T86","obj":"http://purl.org/sig/ont/fma/fma62873"},{"id":"A87","pred":"fma_id","subj":"T87","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A88","pred":"fma_id","subj":"T88","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A89","pred":"fma_id","subj":"T89","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A90","pred":"fma_id","subj":"T90","obj":"http://purl.org/sig/ont/fma/fma86583"},{"id":"A91","pred":"fma_id","subj":"T91","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A92","pred":"fma_id","subj":"T92","obj":"http://purl.org/sig/ont/fma/fma256135"},{"id":"A93","pred":"fma_id","subj":"T93","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A94","pred":"fma_id","subj":"T94","obj":"http://purl.org/sig/ont/fma/fma84050"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PD-MONDO

LitCovid-PD-CLO

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T210","span":{"begin":35,"end":36},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T211","span":{"begin":412,"end":413},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T212","span":{"begin":709,"end":716},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T213","span":{"begin":765,"end":766},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T214","span":{"begin":811,"end":812},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T215","span":{"begin":816,"end":817},"obj":"http://purl.obolibrary.org/obo/CLO_0001021"},{"id":"T216","span":{"begin":869,"end":875},"obj":"http://purl.obolibrary.org/obo/CL_0000084"},{"id":"T217","span":{"begin":1001,"end":1002},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T218","span":{"begin":1043,"end":1044},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T219","span":{"begin":1098,"end":1099},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T220","span":{"begin":1181,"end":1182},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PD-CHEBI

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T114","span":{"begin":234,"end":236},"obj":"Chemical"},{"id":"T115","span":{"begin":744,"end":748},"obj":"Chemical"},{"id":"T116","span":{"begin":976,"end":978},"obj":"Chemical"},{"id":"T118","span":{"begin":982,"end":984},"obj":"Chemical"},{"id":"T120","span":{"begin":1078,"end":1080},"obj":"Chemical"},{"id":"T121","span":{"begin":1278,"end":1280},"obj":"Chemical"}],"attributes":[{"id":"A114","pred":"chebi_id","subj":"T114","obj":"http://purl.obolibrary.org/obo/CHEBI_73601"},{"id":"A115","pred":"chebi_id","subj":"T115","obj":"http://purl.obolibrary.org/obo/CHEBI_35490"},{"id":"A116","pred":"chebi_id","subj":"T116","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A117","pred":"chebi_id","subj":"T116","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A118","pred":"chebi_id","subj":"T118","obj":"http://purl.obolibrary.org/obo/CHEBI_63895"},{"id":"A119","pred":"chebi_id","subj":"T118","obj":"http://purl.obolibrary.org/obo/CHEBI_74072"},{"id":"A120","pred":"chebi_id","subj":"T120","obj":"http://purl.obolibrary.org/obo/CHEBI_73601"},{"id":"A121","pred":"chebi_id","subj":"T121","obj":"http://purl.obolibrary.org/obo/CHEBI_73601"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PD-HP

{"project":"LitCovid-PD-HP","denotations":[{"id":"T174","span":{"begin":247,"end":252},"obj":"Phenotype"},{"id":"T175","span":{"begin":1013,"end":1027},"obj":"Phenotype"},{"id":"T176","span":{"begin":1301,"end":1315},"obj":"Phenotype"}],"attributes":[{"id":"A174","pred":"hp_id","subj":"T174","obj":"http://purl.obolibrary.org/obo/HP_0031273"},{"id":"A175","pred":"hp_id","subj":"T175","obj":"http://purl.obolibrary.org/obo/HP_0033041"},{"id":"A176","pred":"hp_id","subj":"T176","obj":"http://purl.obolibrary.org/obo/HP_0033041"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PD-GO-BP

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T10","span":{"begin":869,"end":889},"obj":"http://purl.obolibrary.org/obo/GO_0042098"},{"id":"T11","span":{"begin":871,"end":889},"obj":"http://purl.obolibrary.org/obo/GO_0008283"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-sentences

{"project":"LitCovid-sentences","denotations":[{"id":"T171","span":{"begin":0,"end":64},"obj":"Sentence"},{"id":"T172","span":{"begin":65,"end":279},"obj":"Sentence"},{"id":"T173","span":{"begin":280,"end":492},"obj":"Sentence"},{"id":"T174","span":{"begin":493,"end":654},"obj":"Sentence"},{"id":"T175","span":{"begin":655,"end":833},"obj":"Sentence"},{"id":"T176","span":{"begin":834,"end":1033},"obj":"Sentence"},{"id":"T177","span":{"begin":1034,"end":1295},"obj":"Sentence"},{"id":"T178","span":{"begin":1296,"end":1422},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PMC-OGER-BB

{"project":"LitCovid-PMC-OGER-BB","denotations":[{"id":"T376","span":{"begin":4,"end":14},"obj":"SP_7"},{"id":"T377","span":{"begin":319,"end":327},"obj":"SP_7"},{"id":"T378","span":{"begin":468,"end":474},"obj":"UBERON:0002405"},{"id":"T379","span":{"begin":611,"end":621},"obj":"SP_7"},{"id":"T380","span":{"begin":622,"end":625},"obj":"GO:0071735"},{"id":"T381","span":{"begin":640,"end":643},"obj":"GO:0071735"},{"id":"T382","span":{"begin":709,"end":716},"obj":"CL:0000084"},{"id":"T383","span":{"begin":744,"end":750},"obj":"PR:000029027"},{"id":"T384","span":{"begin":819,"end":831},"obj":"CHEBI:17076;CHEBI:17076"},{"id":"T385","span":{"begin":869,"end":875},"obj":"CL:0000084;GO:0042098"},{"id":"T386","span":{"begin":876,"end":889},"obj":"GO:0042098"},{"id":"T387","span":{"begin":982,"end":986},"obj":"PR:000001393"},{"id":"T388","span":{"begin":992,"end":997},"obj":"PR:000000017"},{"id":"T71374","span":{"begin":4,"end":14},"obj":"SP_7"},{"id":"T29483","span":{"begin":319,"end":327},"obj":"SP_7"},{"id":"T59082","span":{"begin":468,"end":474},"obj":"UBERON:0002405"},{"id":"T61047","span":{"begin":611,"end":621},"obj":"SP_7"},{"id":"T85640","span":{"begin":622,"end":625},"obj":"GO:0071735"},{"id":"T43262","span":{"begin":640,"end":643},"obj":"GO:0071735"},{"id":"T96002","span":{"begin":709,"end":716},"obj":"CL:0000084"},{"id":"T52401","span":{"begin":744,"end":750},"obj":"PR:000029027"},{"id":"T37931","span":{"begin":819,"end":831},"obj":"CHEBI:17076;CHEBI:17076"},{"id":"T58468","span":{"begin":869,"end":875},"obj":"CL:0000084;GO:0042098"},{"id":"T37970","span":{"begin":876,"end":889},"obj":"GO:0042098"},{"id":"T39326","span":{"begin":982,"end":986},"obj":"PR:000001393"},{"id":"T780","span":{"begin":992,"end":997},"obj":"PR:000000017"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

LitCovid-PubTator

2_test

{"project":"2_test","denotations":[{"id":"32535093-25971393-4828880","span":{"begin":1029,"end":1031},"obj":"25971393"}],"text":"How SARS-CoV-2 infection may cause a hyperinflammatory syndrome? At this point we can only formulate hypotheses, based on the clinical picture of the observed patients and using other diseases with overlapping manifestations, such as KD and Toxic Shock Syndrome (TSS), as models. The delay between the pandemic peak of COVID-19 and the occurrence of this hyperinflammatory syndrome in children does not point to a direct effect of the infection, but rather towards an immune-mediated disease. This seems to be confirmed also by the observation of Verdoni et al. that the majority of their patients had positive SARS-CoV-2 IgG, but negative IgM and swabs. Staphylococcal or Streptococcal TSS are the result of T cells induction by superantigens TSST-1, enterotoxins B or C (staphylococci), or pyrogenic exotoxin A or B (streptococci). Superantigens can stimulate clonal T cell proliferation and this leads to the production of massive amounts of pro-inflammatory cytokines, as IL-1, IL-6, and IFN-γ in a so-called cytokine storm [76]. There is a body of evidence suggesting that KD may be caused by a superantigen response, and recent data demonstrated that KSS is characterized by a massive pro-inflammatory cytokine release that differentiate those patients from the “regular” KD patients [77]. This cytokine storm could be the underlying mechanism leading to the clinical picture similar of that of TSS, KSS, and PeCOHS."}

PMC:7289100 / 26160-27582 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:7289100 / 26160-27582 JSON TXT