PMC:7281546 / 47242-47941 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T268","span":{"begin":79,"end":88},"obj":"Body_part"},{"id":"T269","span":{"begin":201,"end":206},"obj":"Body_part"},{"id":"T270","span":{"begin":275,"end":284},"obj":"Body_part"}],"attributes":[{"id":"A268","pred":"fma_id","subj":"T268","obj":"http://purl.org/sig/ont/fma/fma84050"},{"id":"A269","pred":"fma_id","subj":"T269","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A270","pred":"fma_id","subj":"T270","obj":"http://purl.org/sig/ont/fma/fma84050"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T111","span":{"begin":0,"end":15},"obj":"Disease"},{"id":"T112","span":{"begin":6,"end":15},"obj":"Disease"},{"id":"T113","span":{"begin":318,"end":339},"obj":"Disease"}],"attributes":[{"id":"A111","pred":"mondo_id","subj":"T111","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A112","pred":"mondo_id","subj":"T112","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A113","pred":"mondo_id","subj":"T113","obj":"http://purl.obolibrary.org/obo/MONDO_0021166"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T448","span":{"begin":201,"end":206},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T449","span":{"begin":457,"end":458},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T450","span":{"begin":494,"end":495},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T451","span":{"begin":595,"end":602},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T378","span":{"begin":542,"end":551},"obj":"Chemical"}],"attributes":[{"id":"A378","pred":"chebi_id","subj":"T378","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T339","span":{"begin":0,"end":15},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T340","span":{"begin":30,"end":45},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T341","span":{"begin":79,"end":100},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T342","span":{"begin":167,"end":184},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T343","span":{"begin":167,"end":184},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T344","span":{"begin":370,"end":379},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T345","span":{"begin":370,"end":379},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T346","span":{"begin":542,"end":574},"obj":"http://purl.obolibrary.org/obo/GO_0140374"},{"id":"T347","span":{"begin":552,"end":574},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T348","span":{"begin":559,"end":574},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T349","span":{"begin":646,"end":655},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T350","span":{"begin":646,"end":655},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T351","span":{"begin":681,"end":698},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T352","span":{"begin":681,"end":698},"obj":"http://purl.obolibrary.org/obo/GO_0019058"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-sentences","denotations":[{"id":"T352","span":{"begin":0,"end":101},"obj":"Sentence"},{"id":"T353","span":{"begin":102,"end":207},"obj":"Sentence"},{"id":"T354","span":{"begin":208,"end":340},"obj":"Sentence"},{"id":"T355","span":{"begin":341,"end":428},"obj":"Sentence"},{"id":"T356","span":{"begin":429,"end":581},"obj":"Sentence"},{"id":"T357","span":{"begin":582,"end":699},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"2_test","denotations":[{"id":"32403318-28690332-82827498","span":{"begin":576,"end":579},"obj":"28690332"}],"text":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}

{"project":"LitCovid-PubTator","denotations":[{"id":"1596","span":{"begin":0,"end":15},"obj":"Disease"},{"id":"1597","span":{"begin":192,"end":200},"obj":"Disease"}],"attributes":[{"id":"A1596","pred":"tao:has_database_id","subj":"1596","obj":"MESH:D001102"},{"id":"A1597","pred":"tao:has_database_id","subj":"1597","obj":"MESH:D007239"}],"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":"Viral infection triggers host immune response to induce IFNs’ and inflammatory cytokines’ production. Released IFNs elicit the expression of numerous ISGs which limit viral replication in the infected cells. However, the release of excessive amounts of IFNs and inflammatory cytokines will lead to autoimmune and auto-inflammatory diseases. The concomitant uncontrolled apoptosis is also one outcome that is harmful to the host. To maintain the reaction in a proper balance, hosts have evolved a series of effective mechanisms to control the antiviral innate immune response [230]. In contrast, viruses often break this balance, causing improper apoptosis reaction, which benefits viral replication."}