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2_test

{"project":"2_test","denotations":[{"id":"22496647-21297424-98010798","span":{"begin":326,"end":328},"obj":"21297424"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

pmc-enju-pas

bionlp-st-ge-2016-test-proteins

{"project":"bionlp-st-ge-2016-test-proteins","denotations":[{"id":"T13722","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T13721","span":{"begin":387,"end":392},"obj":"Protein"}],"namespaces":[{"prefix":"_base","uri":"http://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

bionlp-st-ge-2016-uniprot

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T14061","span":{"begin":1611,"end":1616},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14060","span":{"begin":1356,"end":1361},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14059","span":{"begin":1290,"end":1295},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14058","span":{"begin":1124,"end":1129},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14057","span":{"begin":647,"end":652},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14056","span":{"begin":560,"end":565},"obj":"http://www.uniprot.org/uniprot/O94916"},{"id":"T14055","span":{"begin":387,"end":392},"obj":"http://www.uniprot.org/uniprot/O94916"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T13723","span":{"begin":992,"end":1007},"obj":"http://purl.obolibrary.org/obo/GO_0016032"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

GO-MF

{"project":"GO-MF","denotations":[{"id":"T13730","span":{"begin":1496,"end":1509},"obj":"http://purl.obolibrary.org/obo/GO_0051059"},{"id":"T13729","span":{"begin":1617,"end":1624},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T13728","span":{"begin":1502,"end":1509},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T13727","span":{"begin":1362,"end":1369},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T13726","span":{"begin":653,"end":660},"obj":"http://purl.obolibrary.org/obo/GO_0005488"},{"id":"T13725","span":{"begin":566,"end":573},"obj":"http://purl.obolibrary.org/obo/GO_0005488"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

sentences

{"project":"sentences","denotations":[{"id":"T13714","span":{"begin":1463,"end":1694},"obj":"Sentence"},{"id":"T13713","span":{"begin":1147,"end":1462},"obj":"Sentence"},{"id":"T13712","span":{"begin":977,"end":1146},"obj":"Sentence"},{"id":"T13711","span":{"begin":626,"end":976},"obj":"Sentence"},{"id":"T13710","span":{"begin":443,"end":625},"obj":"Sentence"},{"id":"T13709","span":{"begin":337,"end":442},"obj":"Sentence"},{"id":"T13708","span":{"begin":110,"end":336},"obj":"Sentence"},{"id":"T13707","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"T219","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"T220","span":{"begin":110,"end":336},"obj":"Sentence"},{"id":"T221","span":{"begin":337,"end":442},"obj":"Sentence"},{"id":"T222","span":{"begin":443,"end":625},"obj":"Sentence"},{"id":"T223","span":{"begin":626,"end":763},"obj":"Sentence"},{"id":"T224","span":{"begin":764,"end":976},"obj":"Sentence"},{"id":"T225","span":{"begin":977,"end":1146},"obj":"Sentence"},{"id":"T226","span":{"begin":1147,"end":1462},"obj":"Sentence"},{"id":"T227","span":{"begin":1463,"end":1694},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

ICD10

{"project":"ICD10","denotations":[{"id":"T13724","span":{"begin":992,"end":1007},"obj":"http://purl.bioontology.org/ontology/ICD10/B34.9"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

simple1

{"project":"simple1","denotations":[{"id":"T13736","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T13735","span":{"begin":387,"end":392},"obj":"Protein"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

BioNLP16_DUT

{"project":"BioNLP16_DUT","denotations":[{"id":"T14444","span":{"begin":1597,"end":1607},"obj":"Negative_regulation"},{"id":"T14443","span":{"begin":1617,"end":1624},"obj":"Binding"},{"id":"T14442","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T14441","span":{"begin":387,"end":392},"obj":"Protein"}],"relations":[{"id":"R10801","pred":"themeOf","subj":"T14442","obj":"T14443"},{"id":"R10802","pred":"themeOf","subj":"T14443","obj":"T14444"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

BioNLP16_Messiy

{"project":"BioNLP16_Messiy","denotations":[{"id":"T14074","span":{"begin":1617,"end":1624},"obj":"Binding"},{"id":"T14073","span":{"begin":1597,"end":1607},"obj":"Negative_regulation"},{"id":"T14072","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T14071","span":{"begin":387,"end":392},"obj":"Protein"}],"relations":[{"id":"R10464","pred":"themeOf","subj":"T14072","obj":"T14074"},{"id":"R10465","pred":"themeOf","subj":"T14074","obj":"T14073"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

DLUT931

{"project":"DLUT931","denotations":[{"id":"T14066","span":{"begin":1597,"end":1607},"obj":"Negative_regulation"},{"id":"T14065","span":{"begin":1617,"end":1624},"obj":"Binding"},{"id":"T14064","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T14063","span":{"begin":387,"end":392},"obj":"Protein"}],"relations":[{"id":"R10462","pred":"themeOf","subj":"T14064","obj":"T14065"},{"id":"R10463","pred":"themeOf","subj":"T14065","obj":"T14066"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

bionlp-st-ge-2016-test-ihmc

bionlp-st-ge-2016-spacy-parsed

bionlp-st-ge-2016-test-tees

{"project":"bionlp-st-ge-2016-test-tees","denotations":[{"id":"T14093","span":{"begin":1617,"end":1624},"obj":"Binding"},{"id":"T14092","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T14091","span":{"begin":1496,"end":1501},"obj":"Protein"},{"id":"T14090","span":{"begin":1345,"end":1352},"obj":"Negative_regulation"},{"id":"T14089","span":{"begin":1356,"end":1375},"obj":"Protein"},{"id":"T14088","span":{"begin":1296,"end":1299},"obj":"Protein"},{"id":"T14087","span":{"begin":1290,"end":1295},"obj":"Protein"},{"id":"T14086","span":{"begin":1130,"end":1133},"obj":"Protein"},{"id":"T14085","span":{"begin":1124,"end":1129},"obj":"Protein"},{"id":"T14084","span":{"begin":647,"end":652},"obj":"Protein"},{"id":"T14083","span":{"begin":601,"end":606},"obj":"Protein"},{"id":"T14082","span":{"begin":560,"end":579},"obj":"Protein"},{"id":"T14081","span":{"begin":387,"end":392},"obj":"Protein"},{"id":"T14080","span":{"begin":157,"end":168},"obj":"Protein"},{"id":"T14079","span":{"begin":110,"end":124},"obj":"Protein"},{"id":"T14078","span":{"begin":53,"end":59},"obj":"Positive_regulation"},{"id":"T14077","span":{"begin":67,"end":85},"obj":"Protein"},{"id":"T14076","span":{"begin":26,"end":39},"obj":"Protein"}],"relations":[{"id":"R10466","pred":"causeOf","subj":"T14076","obj":"T14078"},{"id":"R10467","pred":"themeOf","subj":"T14077","obj":"T14078"},{"id":"R10468","pred":"themeOf","subj":"T14089","obj":"T14090"},{"id":"R10469","pred":"themeOf","subj":"T14092","obj":"T14093"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

testone

{"project":"testone","denotations":[{"id":"T13699","span":{"begin":1597,"end":1607},"obj":"Negative_regulation"},{"id":"T13698","span":{"begin":1244,"end":1253},"obj":"Positive_regulation"},{"id":"T13697","span":{"begin":629,"end":638},"obj":"Negative_regulation"},{"id":"T13696","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T13695","span":{"begin":387,"end":392},"obj":"Protein"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

test3

{"project":"test3","denotations":[{"id":"T13705","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T13704","span":{"begin":387,"end":392},"obj":"Protein"},{"id":"T13702","span":{"begin":1611,"end":1616},"obj":"Protein"},{"id":"T13701","span":{"begin":387,"end":392},"obj":"Protein"}],"text":"As shown in Figure 1, the subtype C LTR was the most active of the HIV-1 LTR subtypes in the reporter assays. Subtype C LTRs generally have three functional NF-κB sites in their LTRs, and subtype C is the predominant viral subtype in the African and Asian HIV-1 epidemics where MTb co-infection is extremely common [1], [2], [28], [52]. We thus next extended our analysis of the role of NFAT5 in MTb/HIV-1 co-infection to a subtype C isolate. We first constructed an infectious molecular clone of the HIV-1 subtype C primary isolate HIV-198IN22, which has two NFAT5 binding sites in its LTR and three NF-κB sites (Figure 6A). We disrupted the two NFAT5 binding sites by changing the TT of each site to CC to create a mutant virus that we named HIV-198IN22-N5-Mut. Bulk PBMC from four normal donors were infected overnight with 1000 TCID50 of wild-type HIV-198IN22 or HIV-198IN22-N5-Mut and the cultures were then co-infected with MTb CDC1551 or left infected with virus alone. At day 11 post-viral infection, wild-type HIV-198IN22 replication was greater, but not significantly so, as compared to replication of HIV-198IN22 NFAT5-Mut (Figure 6B). However, in the context of MTb co-infection, wild-type HIV-198IN22 replication was significantly increased (p\u003c0.05) at day 11 over HIV-198IN22 NFAT5-Mut replication (Figure 6C), indicating that the absence of NFAT5 binding sites was particularly detrimental to virus replication in the presence of MTb co-infection. Thus, even when three functional NF-κB binding sites are present in the LTR, as in the HIV-1 subtype C infectious clone studied here, disruption of NFAT5 binding to the LTR impairs virus replication in response to MTb co-infection."}

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