PMC:7281546 / 47213-48795 JSONTXT

{"project":"LitCovid-PD-FMA-UBERON","denotations":[{"id":"T268","span":{"begin":108,"end":117},"obj":"Body_part"},{"id":"T269","span":{"begin":230,"end":235},"obj":"Body_part"},{"id":"T270","span":{"begin":304,"end":313},"obj":"Body_part"},{"id":"T271","span":{"begin":755,"end":760},"obj":"Body_part"},{"id":"T272","span":{"begin":873,"end":877},"obj":"Body_part"},{"id":"T273","span":{"begin":1311,"end":1318},"obj":"Body_part"},{"id":"T274","span":{"begin":1349,"end":1353},"obj":"Body_part"},{"id":"T275","span":{"begin":1404,"end":1412},"obj":"Body_part"},{"id":"T276","span":{"begin":1465,"end":1469},"obj":"Body_part"},{"id":"T277","span":{"begin":1495,"end":1502},"obj":"Body_part"},{"id":"T278","span":{"begin":1528,"end":1535},"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"},{"id":"A271","pred":"fma_id","subj":"T271","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A272","pred":"fma_id","subj":"T272","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A273","pred":"fma_id","subj":"T273","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A274","pred":"fma_id","subj":"T274","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A275","pred":"fma_id","subj":"T275","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A276","pred":"fma_id","subj":"T276","obj":"http://purl.org/sig/ont/fma/fma68646"},{"id":"A277","pred":"fma_id","subj":"T277","obj":"http://purl.org/sig/ont/fma/fma67257"},{"id":"A278","pred":"fma_id","subj":"T278","obj":"http://purl.org/sig/ont/fma/fma67257"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"LitCovid-PD-MONDO","denotations":[{"id":"T111","span":{"begin":29,"end":44},"obj":"Disease"},{"id":"T112","span":{"begin":35,"end":44},"obj":"Disease"},{"id":"T113","span":{"begin":347,"end":368},"obj":"Disease"},{"id":"T114","span":{"begin":1061,"end":1070},"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"},{"id":"A114","pred":"mondo_id","subj":"T114","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"LitCovid-PD-CLO","denotations":[{"id":"T448","span":{"begin":230,"end":235},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T449","span":{"begin":486,"end":487},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T450","span":{"begin":523,"end":524},"obj":"http://purl.obolibrary.org/obo/CLO_0001020"},{"id":"T451","span":{"begin":624,"end":631},"obj":"http://purl.obolibrary.org/obo/NCBITaxon_10239"},{"id":"T452","span":{"begin":755,"end":760},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T453","span":{"begin":771,"end":775},"obj":"http://purl.obolibrary.org/obo/CLO_0009524"},{"id":"T454","span":{"begin":771,"end":775},"obj":"http://purl.obolibrary.org/obo/CLO_0050515"},{"id":"T455","span":{"begin":777,"end":782},"obj":"http://purl.obolibrary.org/obo/CLO_0050908"},{"id":"T456","span":{"begin":787,"end":795},"obj":"http://purl.obolibrary.org/obo/CLO_0007536"},{"id":"T457","span":{"begin":873,"end":877},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T458","span":{"begin":878,"end":881},"obj":"http://purl.obolibrary.org/obo/CLO_0051582"},{"id":"T459","span":{"begin":966,"end":976},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T460","span":{"begin":1022,"end":1027},"obj":"http://purl.obolibrary.org/obo/CLO_0001313"},{"id":"T461","span":{"begin":1050,"end":1053},"obj":"http://purl.obolibrary.org/obo/CLO_0001203"},{"id":"T462","span":{"begin":1114,"end":1124},"obj":"http://purl.obolibrary.org/obo/CLO_0001658"},{"id":"T463","span":{"begin":1319,"end":1321},"obj":"http://purl.obolibrary.org/obo/CLO_0050050"},{"id":"T464","span":{"begin":1349,"end":1353},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T465","span":{"begin":1417,"end":1421},"obj":"http://purl.obolibrary.org/obo/CLO_0008149"},{"id":"T466","span":{"begin":1423,"end":1425},"obj":"http://purl.obolibrary.org/obo/CLO_0008922"},{"id":"T467","span":{"begin":1423,"end":1425},"obj":"http://purl.obolibrary.org/obo/CLO_0050052"},{"id":"T468","span":{"begin":1465,"end":1469},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T469","span":{"begin":1492,"end":1494},"obj":"http://purl.obolibrary.org/obo/CLO_0050050"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"LitCovid-PD-CHEBI","denotations":[{"id":"T378","span":{"begin":571,"end":580},"obj":"Chemical"},{"id":"T379","span":{"begin":777,"end":779},"obj":"Chemical"},{"id":"T380","span":{"begin":1222,"end":1225},"obj":"Chemical"},{"id":"T383","span":{"begin":1226,"end":1232},"obj":"Chemical"},{"id":"T385","span":{"begin":1245,"end":1249},"obj":"Chemical"},{"id":"T386","span":{"begin":1311,"end":1318},"obj":"Chemical"},{"id":"T387","span":{"begin":1404,"end":1412},"obj":"Chemical"},{"id":"T388","span":{"begin":1423,"end":1425},"obj":"Chemical"},{"id":"T389","span":{"begin":1495,"end":1502},"obj":"Chemical"},{"id":"T390","span":{"begin":1528,"end":1535},"obj":"Chemical"}],"attributes":[{"id":"A378","pred":"chebi_id","subj":"T378","obj":"http://purl.obolibrary.org/obo/CHEBI_22587"},{"id":"A379","pred":"chebi_id","subj":"T379","obj":"http://purl.obolibrary.org/obo/CHEBI_74792"},{"id":"A380","pred":"chebi_id","subj":"T380","obj":"http://purl.obolibrary.org/obo/CHEBI_16761"},{"id":"A381","pred":"chebi_id","subj":"T380","obj":"http://purl.obolibrary.org/obo/CHEBI_456216"},{"id":"A382","pred":"chebi_id","subj":"T380","obj":"http://purl.obolibrary.org/obo/CHEBI_73342"},{"id":"A383","pred":"chebi_id","subj":"T383","obj":"http://purl.obolibrary.org/obo/CHEBI_33942"},{"id":"A384","pred":"chebi_id","subj":"T383","obj":"http://purl.obolibrary.org/obo/CHEBI_47013"},{"id":"A385","pred":"chebi_id","subj":"T385","obj":"http://purl.obolibrary.org/obo/CHEBI_62913"},{"id":"A386","pred":"chebi_id","subj":"T386","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A387","pred":"chebi_id","subj":"T387","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A388","pred":"chebi_id","subj":"T388","obj":"http://purl.obolibrary.org/obo/CHEBI_29387"},{"id":"A389","pred":"chebi_id","subj":"T389","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"},{"id":"A390","pred":"chebi_id","subj":"T390","obj":"http://purl.obolibrary.org/obo/CHEBI_36080"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"LitCovid-PD-GO-BP","denotations":[{"id":"T337","span":{"begin":19,"end":28},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T338","span":{"begin":19,"end":28},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T339","span":{"begin":29,"end":44},"obj":"http://purl.obolibrary.org/obo/GO_0016032"},{"id":"T340","span":{"begin":59,"end":74},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T341","span":{"begin":108,"end":129},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T342","span":{"begin":196,"end":213},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T343","span":{"begin":196,"end":213},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T344","span":{"begin":399,"end":408},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T345","span":{"begin":399,"end":408},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T346","span":{"begin":571,"end":603},"obj":"http://purl.obolibrary.org/obo/GO_0140374"},{"id":"T347","span":{"begin":581,"end":603},"obj":"http://purl.obolibrary.org/obo/GO_0045087"},{"id":"T348","span":{"begin":588,"end":603},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T349","span":{"begin":675,"end":684},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T350","span":{"begin":675,"end":684},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T351","span":{"begin":710,"end":727},"obj":"http://purl.obolibrary.org/obo/GO_0019079"},{"id":"T352","span":{"begin":710,"end":727},"obj":"http://purl.obolibrary.org/obo/GO_0019058"},{"id":"T353","span":{"begin":847,"end":856},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T354","span":{"begin":847,"end":856},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T355","span":{"begin":933,"end":942},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T356","span":{"begin":933,"end":942},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T357","span":{"begin":1153,"end":1162},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T358","span":{"begin":1153,"end":1162},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T359","span":{"begin":1267,"end":1298},"obj":"http://purl.obolibrary.org/obo/GO_0030264"},{"id":"T360","span":{"begin":1354,"end":1363},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T361","span":{"begin":1354,"end":1363},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T362","span":{"begin":1470,"end":1479},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T363","span":{"begin":1470,"end":1479},"obj":"http://purl.obolibrary.org/obo/GO_0006915"},{"id":"T364","span":{"begin":1550,"end":1559},"obj":"http://purl.obolibrary.org/obo/GO_0097194"},{"id":"T365","span":{"begin":1550,"end":1559},"obj":"http://purl.obolibrary.org/obo/GO_0006915"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"LitCovid-sentences","denotations":[{"id":"T350","span":{"begin":0,"end":4},"obj":"Sentence"},{"id":"T351","span":{"begin":5,"end":28},"obj":"Sentence"},{"id":"T352","span":{"begin":29,"end":130},"obj":"Sentence"},{"id":"T353","span":{"begin":131,"end":236},"obj":"Sentence"},{"id":"T354","span":{"begin":237,"end":369},"obj":"Sentence"},{"id":"T355","span":{"begin":370,"end":457},"obj":"Sentence"},{"id":"T356","span":{"begin":458,"end":610},"obj":"Sentence"},{"id":"T357","span":{"begin":611,"end":728},"obj":"Sentence"},{"id":"T358","span":{"begin":729,"end":833},"obj":"Sentence"},{"id":"T359","span":{"begin":834,"end":932},"obj":"Sentence"},{"id":"T360","span":{"begin":933,"end":1055},"obj":"Sentence"},{"id":"T361","span":{"begin":1056,"end":1299},"obj":"Sentence"},{"id":"T362","span":{"begin":1300,"end":1480},"obj":"Sentence"},{"id":"T363","span":{"begin":1481,"end":1582},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

{"project":"2_test","denotations":[{"id":"32403318-28690332-82827498","span":{"begin":605,"end":608},"obj":"28690332"},{"id":"32403318-17082813-82827499","span":{"begin":1050,"end":1053},"obj":"17082813"},{"id":"32403318-30404647-82827500","span":{"begin":1577,"end":1580},"obj":"30404647"}],"text":"4.3. Modulation of Apoptosis\nViral 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.\nPEDV infects various host cells including Vero, PK-15 and Marc-145 and cause obvious cytopathic effects. PEDV-induced apoptosis of the infected cell has been demonstrated both in vitro and in vivo [231]. Apoptosis is induced through the activation of apoptotic caspases, including caspase-2, -3, -6, -7, -8, -9, and -10 [232]. PEDV infection results in obvious caspase-3 and caspase-8 activation, as well as the cleavage of apoptosis-inducing factor mitochondria-associated 1 (AIFM1) and poly ADP-ribose polymerase (PARP), which leads to apoptotic nuclear fragmentation. PEDV spike protein S1 significantly elicits host cell apoptosis, while the nsp1–16 and other structural proteins (M, N, E, S2, and ORF3) have none or few effects on cell apoptosis. Therefore, S1 protein is probably the critical protein mediating the apoptosis induced by PEDV [128]."}

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