Biomarker-guided tuberculosis preventive therapy (CORTIS): a randomised controlled trial
Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid th...
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| Published in | The Lancet infectious diseases Vol. 21; no. 3; pp. 354 - 365 |
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| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Ltd
01.03.2021
Elsevier B.V Elsevier Limited Elsevier Science ;, The Lancet Pub. Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid three-group study design.
Adult volunteers aged 18–59 years were recruited at five geographically distinct communities in South Africa. Whole blood was sampled for RISK11 by quantitative RT-PCR assay from eligible volunteers without HIV, recent previous tuberculosis (ie, <3 years before screening), or comorbidities at screening. RISK11-positive participants were block randomised (1:2; block size 15) to once-weekly, directly-observed, open-label isoniazid and rifapentine for 12 weeks (ie, RISK11 positive and 3HP positive), or no treatment (ie, RISK11 positive and 3HP negative). A subset of eligible RISK11-negative volunteers were randomly assigned to no treatment (ie, RISK11 negative and 3HP negative). Diagnostic discrimination of prevalent tuberculosis was tested in all participants at baseline. Thereafter, prognostic discrimination of incident tuberculosis was tested in the untreated RISK11-positive versus RISK11-negative groups, and treatment efficacy in the 3HP-treated versus untreated RISK11-positive groups, during active surveillance through 15 months. The primary endpoint was microbiologically confirmed pulmonary tuberculosis. The primary outcome measures were risk ratio [RR] for tuberculosis of RISK11-positive to RISK11-negative participants, and treatment efficacy. This trial is registered with ClinicalTrials.gov, NCT02735590.
20 207 volunteers were screened, and 2923 participants were enrolled, including RISK11-positive participants randomly assigned to 3HP (n=375) or no 3HP (n=764), and 1784 RISK11-negative participants. Cumulative probability of prevalent or incident tuberculosis disease was 0·066 (95% CI 0·049 to 0·084) in RISK11-positive (3HP negative) participants and 0·018 (0·011 to 0·025) in RISK11-negative participants (RR 3·69, 95% CI 2·25–6·05) over 15 months. Tuberculosis prevalence was 47 (4·1%) of 1139 versus 14 (0·78%) of 1984 in RISK11-positive compared with RISK11-negative participants, respectively (diagnostic RR 5·13, 95% CI 2·93 to 9·43). Tuberculosis incidence over 15 months was 2·09 (95% CI 0·97 to 3·19) vs 0·80 (0·30 to 1·30) per 100 person years in RISK11-positive (3HP-negative) participants compared with RISK11-negative participants (cumulative incidence ratio 2·6, 95% CI 1·2 to 5·9). Serious adverse events related to 3HP included one hospitalisation for seizures (unintentional isoniazid overdose) and one death of unknown cause (possibly temporally related). Tuberculosis incidence over 15 months was 1·94 (95% CI 0·35 to 3·50) versus 2·09 (95% CI 0·97 to 3·19) per 100 person-years in 3HP-treated RISK11-positive participants compared with untreated RISK11-positive participants (efficacy 7·0%, 95% CI −145 to 65).
The RISK11 signature discriminated between individuals with prevalent tuberculosis, or progression to incident tuberculosis, and individuals who remained healthy, but provision of 3HP to signature-positive individuals after exclusion of baseline disease did not reduce progression to tuberculosis over 15 months.
Bill and Melinda Gates Foundation, South African Medical Research Council. |
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| AbstractList | BACKGROUNDTargeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid three-group study design. METHODSAdult volunteers aged 18-59 years were recruited at five geographically distinct communities in South Africa. Whole blood was sampled for RISK11 by quantitative RT-PCR assay from eligible volunteers without HIV, recent previous tuberculosis (ie, <3 years before screening), or comorbidities at screening. RISK11-positive participants were block randomised (1:2; block size 15) to once-weekly, directly-observed, open-label isoniazid and rifapentine for 12 weeks (ie, RISK11 positive and 3HP positive), or no treatment (ie, RISK11 positive and 3HP negative). A subset of eligible RISK11-negative volunteers were randomly assigned to no treatment (ie, RISK11 negative and 3HP negative). Diagnostic discrimination of prevalent tuberculosis was tested in all participants at baseline. Thereafter, prognostic discrimination of incident tuberculosis was tested in the untreated RISK11-positive versus RISK11-negative groups, and treatment efficacy in the 3HP-treated versus untreated RISK11-positive groups, during active surveillance through 15 months. The primary endpoint was microbiologically confirmed pulmonary tuberculosis. The primary outcome measures were risk ratio [RR] for tuberculosis of RISK11-positive to RISK11-negative participants, and treatment efficacy. This trial is registered with ClinicalTrials.gov, NCT02735590. FINDINGS20 207 volunteers were screened, and 2923 participants were enrolled, including RISK11-positive participants randomly assigned to 3HP (n=375) or no 3HP (n=764), and 1784 RISK11-negative participants. Cumulative probability of prevalent or incident tuberculosis disease was 0·066 (95% CI 0·049 to 0·084) in RISK11-positive (3HP negative) participants and 0·018 (0·011 to 0·025) in RISK11-negative participants (RR 3·69, 95% CI 2·25-6·05) over 15 months. Tuberculosis prevalence was 47 (4·1%) of 1139 versus 14 (0·78%) of 1984 in RISK11-positive compared with RISK11-negative participants, respectively (diagnostic RR 5·13, 95% CI 2·93 to 9·43). Tuberculosis incidence over 15 months was 2·09 (95% CI 0·97 to 3·19) vs 0·80 (0·30 to 1·30) per 100 person years in RISK11-positive (3HP-negative) participants compared with RISK11-negative participants (cumulative incidence ratio 2·6, 95% CI 1·2 to 5·9). Serious adverse events related to 3HP included one hospitalisation for seizures (unintentional isoniazid overdose) and one death of unknown cause (possibly temporally related). Tuberculosis incidence over 15 months was 1·94 (95% CI 0·35 to 3·50) versus 2·09 (95% CI 0·97 to 3·19) per 100 person-years in 3HP-treated RISK11-positive participants compared with untreated RISK11-positive participants (efficacy 7·0%, 95% CI -145 to 65). INTERPRETATIONThe RISK11 signature discriminated between individuals with prevalent tuberculosis, or progression to incident tuberculosis, and individuals who remained healthy, but provision of 3HP to signature-positive individuals after exclusion of baseline disease did not reduce progression to tuberculosis over 15 months. FUNDINGBill and Melinda Gates Foundation, South African Medical Research Council. Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid three-group study design. Adult volunteers aged 18-59 years were recruited at five geographically distinct communities in South Africa. Whole blood was sampled for RISK11 by quantitative RT-PCR assay from eligible volunteers without HIV, recent previous tuberculosis (ie, <3 years before screening), or comorbidities at screening. RISK11-positive participants were block randomised (1:2; block size 15) to once-weekly, directly-observed, open-label isoniazid and rifapentine for 12 weeks (ie, RISK11 positive and 3HP positive), or no treatment (ie, RISK11 positive and 3HP negative). A subset of eligible RISK11-negative volunteers were randomly assigned to no treatment (ie, RISK11 negative and 3HP negative). Diagnostic discrimination of prevalent tuberculosis was tested in all participants at baseline. Thereafter, prognostic discrimination of incident tuberculosis was tested in the untreated RISK11-positive versus RISK11-negative groups, and treatment efficacy in the 3HP-treated versus untreated RISK11-positive groups, during active surveillance through 15 months. The primary endpoint was microbiologically confirmed pulmonary tuberculosis. The primary outcome measures were risk ratio [RR] for tuberculosis of RISK11-positive to RISK11-negative participants, and treatment efficacy. This trial is registered with ClinicalTrials.gov, NCT02735590. 20 207 volunteers were screened, and 2923 participants were enrolled, including RISK11-positive participants randomly assigned to 3HP (n=375) or no 3HP (n=764), and 1784 RISK11-negative participants. Cumulative probability of prevalent or incident tuberculosis disease was 0·066 (95% CI 0·049 to 0·084) in RISK11-positive (3HP negative) participants and 0·018 (0·011 to 0·025) in RISK11-negative participants (RR 3·69, 95% CI 2·25-6·05) over 15 months. Tuberculosis prevalence was 47 (4·1%) of 1139 versus 14 (0·78%) of 1984 in RISK11-positive compared with RISK11-negative participants, respectively (diagnostic RR 5·13, 95% CI 2·93 to 9·43). Tuberculosis incidence over 15 months was 2·09 (95% CI 0·97 to 3·19) vs 0·80 (0·30 to 1·30) per 100 person years in RISK11-positive (3HP-negative) participants compared with RISK11-negative participants (cumulative incidence ratio 2·6, 95% CI 1·2 to 5·9). Serious adverse events related to 3HP included one hospitalisation for seizures (unintentional isoniazid overdose) and one death of unknown cause (possibly temporally related). Tuberculosis incidence over 15 months was 1·94 (95% CI 0·35 to 3·50) versus 2·09 (95% CI 0·97 to 3·19) per 100 person-years in 3HP-treated RISK11-positive participants compared with untreated RISK11-positive participants (efficacy 7·0%, 95% CI -145 to 65). The RISK11 signature discriminated between individuals with prevalent tuberculosis, or progression to incident tuberculosis, and individuals who remained healthy, but provision of 3HP to signature-positive individuals after exclusion of baseline disease did not reduce progression to tuberculosis over 15 months. Bill and Melinda Gates Foundation, South African Medical Research Council. Summary Background Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid three-group study design. Methods Adult volunteers aged 18–59 years were recruited at five geographically distinct communities in South Africa. Whole blood was sampled for RISK11 by quantitative RT-PCR assay from eligible volunteers without HIV, recent previous tuberculosis (ie, <3 years before screening), or comorbidities at screening. RISK11-positive participants were block randomised (1:2; block size 15) to once-weekly, directly-observed, open-label isoniazid and rifapentine for 12 weeks (ie, RISK11 positive and 3HP positive), or no treatment (ie, RISK11 positive and 3HP negative). A subset of eligible RISK11-negative volunteers were randomly assigned to no treatment (ie, RISK11 negative and 3HP negative). Diagnostic discrimination of prevalent tuberculosis was tested in all participants at baseline. Thereafter, prognostic discrimination of incident tuberculosis was tested in the untreated RISK11-positive versus RISK11-negative groups, and treatment efficacy in the 3HP-treated versus untreated RISK11-positive groups, during active surveillance through 15 months. The primary endpoint was microbiologically confirmed pulmonary tuberculosis. The primary outcome measures were risk ratio [RR] for tuberculosis of RISK11-positive to RISK11-negative participants, and treatment efficacy. This trial is registered with ClinicalTrials.gov, NCT02735590. Findings 20 207 volunteers were screened, and 2923 participants were enrolled, including RISK11-positive participants randomly assigned to 3HP (n=375) or no 3HP (n=764), and 1784 RISK11-negative participants. Cumulative probability of prevalent or incident tuberculosis disease was 0·066 (95% CI 0·049 to 0·084) in RISK11-positive (3HP negative) participants and 0·018 (0·011 to 0·025) in RISK11-negative participants (RR 3·69, 95% CI 2·25–6·05) over 15 months. Tuberculosis prevalence was 47 (4·1%) of 1139 versus 14 (0·78%) of 1984 in RISK11-positive compared with RISK11-negative participants, respectively (diagnostic RR 5·13, 95% CI 2·93 to 9·43). Tuberculosis incidence over 15 months was 2·09 (95% CI 0·97 to 3·19) vs 0·80 (0·30 to 1·30) per 100 person years in RISK11-positive (3HP-negative) participants compared with RISK11-negative participants (cumulative incidence ratio 2·6, 95% CI 1·2 to 5·9). Serious adverse events related to 3HP included one hospitalisation for seizures (unintentional isoniazid overdose) and one death of unknown cause (possibly temporally related). Tuberculosis incidence over 15 months was 1·94 (95% CI 0·35 to 3·50) versus 2·09 (95% CI 0·97 to 3·19) per 100 person-years in 3HP-treated RISK11-positive participants compared with untreated RISK11-positive participants (efficacy 7·0%, 95% CI −145 to 65). Interpretation The RISK11 signature discriminated between individuals with prevalent tuberculosis, or progression to incident tuberculosis, and individuals who remained healthy, but provision of 3HP to signature-positive individuals after exclusion of baseline disease did not reduce progression to tuberculosis over 15 months. Funding Bill and Melinda Gates Foundation, South African Medical Research Council. Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested performance of a transcriptomic signature of tuberculosis (RISK11) and efficacy of signature-guided preventive therapy in parallel, using a hybrid three-group study design. Adult volunteers aged 18–59 years were recruited at five geographically distinct communities in South Africa. Whole blood was sampled for RISK11 by quantitative RT-PCR assay from eligible volunteers without HIV, recent previous tuberculosis (ie, <3 years before screening), or comorbidities at screening. RISK11-positive participants were block randomised (1:2; block size 15) to once-weekly, directly-observed, open-label isoniazid and rifapentine for 12 weeks (ie, RISK11 positive and 3HP positive), or no treatment (ie, RISK11 positive and 3HP negative). A subset of eligible RISK11-negative volunteers were randomly assigned to no treatment (ie, RISK11 negative and 3HP negative). Diagnostic discrimination of prevalent tuberculosis was tested in all participants at baseline. Thereafter, prognostic discrimination of incident tuberculosis was tested in the untreated RISK11-positive versus RISK11-negative groups, and treatment efficacy in the 3HP-treated versus untreated RISK11-positive groups, during active surveillance through 15 months. The primary endpoint was microbiologically confirmed pulmonary tuberculosis. The primary outcome measures were risk ratio [RR] for tuberculosis of RISK11-positive to RISK11-negative participants, and treatment efficacy. This trial is registered with ClinicalTrials.gov, NCT02735590. 20 207 volunteers were screened, and 2923 participants were enrolled, including RISK11-positive participants randomly assigned to 3HP (n=375) or no 3HP (n=764), and 1784 RISK11-negative participants. Cumulative probability of prevalent or incident tuberculosis disease was 0·066 (95% CI 0·049 to 0·084) in RISK11-positive (3HP negative) participants and 0·018 (0·011 to 0·025) in RISK11-negative participants (RR 3·69, 95% CI 2·25–6·05) over 15 months. Tuberculosis prevalence was 47 (4·1%) of 1139 versus 14 (0·78%) of 1984 in RISK11-positive compared with RISK11-negative participants, respectively (diagnostic RR 5·13, 95% CI 2·93 to 9·43). Tuberculosis incidence over 15 months was 2·09 (95% CI 0·97 to 3·19) vs 0·80 (0·30 to 1·30) per 100 person years in RISK11-positive (3HP-negative) participants compared with RISK11-negative participants (cumulative incidence ratio 2·6, 95% CI 1·2 to 5·9). Serious adverse events related to 3HP included one hospitalisation for seizures (unintentional isoniazid overdose) and one death of unknown cause (possibly temporally related). Tuberculosis incidence over 15 months was 1·94 (95% CI 0·35 to 3·50) versus 2·09 (95% CI 0·97 to 3·19) per 100 person-years in 3HP-treated RISK11-positive participants compared with untreated RISK11-positive participants (efficacy 7·0%, 95% CI −145 to 65). The RISK11 signature discriminated between individuals with prevalent tuberculosis, or progression to incident tuberculosis, and individuals who remained healthy, but provision of 3HP to signature-positive individuals after exclusion of baseline disease did not reduce progression to tuberculosis over 15 months. Bill and Melinda Gates Foundation, South African Medical Research Council. |
| Audience | Academic |
| Author | Erasmus, Mzwandile Matshego, Selvy Selepe, Pearl Majola, Molly Mabe, Dorah Sayed, Sharfuddin Hiemstra, Andriette Mabasa, Immaculate Chung, Eva Kaskar, Masooda Ni Sein, Ni Hlathi, Senzo Ralph Valley, Habibullah Moswegu, Palesa Scriba, Thomas J Borate, Bhavesh Luphoko, Marillyn Nchwe, Grace Dlamini, Celaphiwe Ratangee, Frances Zietsman, Marietjie Kelepu, Xoliswa Market, Juanita Nel, Maryna Veldsman, Ashley Ledwaba, Hilda Makhubalo, Blossom Baepanye, Tshepiso Malay, Vernon Mulenga, Humphrey Modipa, Sylvester Maasdorp, Elizna Janse van Rensburg, Elba Self, Steven Eyre, Candice Corris, Cara-Mia Herling, Roxane Sanyaka, Nomsa Baepanye, Kesenogile Serake, MG Maharaj, Bhavna Mbipa, Nontsikelelo Cetywayo, Nompumelelo Makoanyane, Mpho White, Richard G Cwele, Thobelani Hikuam, Chris Shezi, Thandiwe Yvonne Nzimande, Sphelele Simo Botes, Natasja Braaf, Samentra Kock, Adrianne Raphela, Rodney Ahlers, Petri Gregg, Yolande Kimbung Mbandi, Stanley Mmotsa, Tsiamo Muller, Dorothy Buhlungu, Sivuyile Khoury, Justine Penn-Nicholson, Adam Stryers, Sonia Shenje, Justin F |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33508224$$D View this record in MEDLINE/PubMed |
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| Contributor | Matshego, Selvy Selepe, Pearl Majola, Molly Mabe, Dorah Sayed, Sharfuddin Mabasa, Immaculate Ni Sein, Ni Hlathi, Senzo Ralph Moswegu, Palesa Luphoko, Marillyn Nchwe, Grace Serake, M G Dlamini, Celaphiwe Zietsman, Marietjie Market, Juanita Nel, Maryna Veldsman, Ashley Ledwaba, Hilda Makhubalo, Blossom Baepanye, Tshepiso Malay, Vernon Mulenga, Humphrey Modipa, Sylvester Janse van Rensburg, Elba Eyre, Candice Corris, Cara-Mia Herling, Roxane Sanyaka, Nomsa Baepanye, Kesenogile Maharaj, Bhavna Mbipa, Nontsikelelo Makoanyane, Mpho Cwele, Thobelani Shezi, Thandiwe Yvonne Nzimande, Sphelele Simo Botes, Natasja Braaf, Samentra Kock, Adrianne Mmotsa, Tsiamo Muller, Dorothy Stryers, Sonia Shenje, Justin Clarke, Ken Mbata, Lungile Fikizolo, Moogo Malefo-Grootboom, Shirley van Aswegen, Amanda Moosa, Atika Carstens, Alida Nielson, Tanya Dlamini, Audrey Nhlangulela, Lindiwe Kafaar, Fazlin Maphanga, Nonhle Bridgette Ntshauba, Tedrius Kunene, Israel Gangat, Alia Gumede, Goodness Khanyisile Feni, Tebogo Luabeya, Angelique Kany Kany Ntoahae, Lawerence Collignon, |
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| References | Darboe, Mbandi, Thompson (bib10) 2018; 108 (bib6) 2017 Frascella, Richards, Sossen (bib14) 2020 (bib5) 2014 Behr, Edelstein, Ramakrishnan (bib1) 2019; 367 Zak, Penn-Nicholson, Scriba (bib8) 2016; 387 Moreira-Teixeira, Tabone, Graham (bib20) 2020; 21 Scriba, Penn-Nicholson, Shankar (bib19) 2017; 13 Turner, Gupta, Tsaliki (bib18) 2020; 8 Sterling, Villarino, Borisov (bib21) 2011; 365 Onozaki, Law, Sismanidis, Zignol, Glaziou, Floyd (bib12) 2015; 20 Drain, Bajema, Dowdy (bib15) 2018; 31 Penn-Nicholson, Scriba, Hatherill, White, Sumner (bib7) 2016; 107 Fiore-Gartland, Carpp, Naidoo (bib2) 2018; 109 Gupta, Turner, Venturini (bib11) 2020; 8 Dowdy, Basu, Andrews (bib17) 2013; 187 Darboe, Mbandi, Naidoo (bib9) 2019; 10 Petruccioli, Scriba, Petrone (bib3) 2016; 48 Gunasekera, Cohen, Gao, Ayles, Godfrey-Faussett, Claassens (bib13) 2020; 24 Tiemersma, van der Werf, Borgdorff, Williams, Nagelkerke (bib16) 2011; 6 Sumner, Scriba, Penn-Nicholson, Hatherill, White (bib4) 2019; 9 33508223 - Lancet Infect Dis. 2021 Mar;21(3):299-300 (10.1016/S1473-3099(20)30914-2_bib5) 2014 Tiemersma (10.1016/S1473-3099(20)30914-2_bib16) 2011; 6 (10.1016/S1473-3099(20)30914-2_bib6) 2017 Gunasekera (10.1016/S1473-3099(20)30914-2_bib13) 2020; 24 Sterling (10.1016/S1473-3099(20)30914-2_bib21) 2011; 365 Petruccioli (10.1016/S1473-3099(20)30914-2_bib3) 2016; 48 Fiore-Gartland (10.1016/S1473-3099(20)30914-2_bib2) 2018; 109 Dowdy (10.1016/S1473-3099(20)30914-2_bib17) 2013; 187 Moreira-Teixeira (10.1016/S1473-3099(20)30914-2_bib20) 2020; 21 Onozaki (10.1016/S1473-3099(20)30914-2_bib12) 2015; 20 Behr (10.1016/S1473-3099(20)30914-2_bib1) 2019; 367 Penn-Nicholson (10.1016/S1473-3099(20)30914-2_bib7) 2016; 107 Zak (10.1016/S1473-3099(20)30914-2_bib8) 2016; 387 Darboe (10.1016/S1473-3099(20)30914-2_bib9) 2019; 10 Darboe (10.1016/S1473-3099(20)30914-2_bib10) 2018; 108 Gupta (10.1016/S1473-3099(20)30914-2_bib11) 2020; 8 Frascella (10.1016/S1473-3099(20)30914-2_bib14) 2020 Turner (10.1016/S1473-3099(20)30914-2_bib18) 2020; 8 Sumner (10.1016/S1473-3099(20)30914-2_bib4) 2019; 9 Drain (10.1016/S1473-3099(20)30914-2_bib15) 2018; 31 Scriba (10.1016/S1473-3099(20)30914-2_bib19) 2017; 13 |
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| Snippet | Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We tested... Summary Background Targeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission.... BACKGROUNDTargeted preventive therapy for individuals at highest risk of incident tuberculosis might impact the epidemic by interrupting transmission. We... |
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| SubjectTerms | Adult Adverse events Analysis Antitubercular Agents - therapeutic use Biomarkers Biomarkers - metabolism Cancer Charities Clinical trials Diagnostic systems Discrimination Disease prevention Drug Administration Schedule Epidemiology Female Gene expression Health services HIV HIV Seronegativity Human immunodeficiency virus Humans Immunology Incidence Infections Infectious diseases Isoniazid Isoniazid - therapeutic use Male Medical research Medicine, Preventive Mycobacterium tuberculosis - genetics Oncology, Experimental Overdose Polymerase chain reaction Preventive health services Reverse Transcriptase Polymerase Chain Reaction Rifampin - analogs & derivatives Rifampin - therapeutic use Rifapentine RNA, Bacterial - metabolism Seizures South Africa - epidemiology Surveillance Therapy Treatment Outcome Tuberculosis Tuberculosis - epidemiology Tuberculosis - genetics Tuberculosis - metabolism Tuberculosis - prevention & control Vaccines Young Adult |
| Title | Biomarker-guided tuberculosis preventive therapy (CORTIS): a randomised controlled trial |
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