Evidence map›Paper›PMID 42454801›Full record

Observational studyMemorias do Instituto Oswaldo Cruz2026

Determinants of HIV-1 virologic suppression in HIV-associated tuberculosis in Brazil.

Felipe Ridolfi, Gustavo Amorim, David W Haas, Maria Arriaga, Cody Staats, Marcelo Cordeiro-Santos, Afrânio L Kritski, Marina C Figueiredo, Bruno B Andrade, Timothy R Sterling and 13 more

Abstract readObservational Study
In one paragraph

Observational study in Memorias do Instituto Oswaldo Cruz, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

Felipe RidolfiVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.ORCID http://orcid.org/0000-0002-3377-1026
Gustavo AmorimVanderbilt University Medical Center, Department of Biostatistics, Nashville, TN, USA.
David W HaasVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.
Maria ArriagaVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.
Cody StaatsVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.
Marcelo Cordeiro-SantosFundação Medicina Tropical Dr Heitor Vieira Dourado, Manaus, AM, Brasil.
Afrânio L KritskiUniversidade Federal do Rio de Janeiro, Faculdade de Medicina, Rio de Janeiro, RJ, Brasil.
Marina C FigueiredoVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.
Bruno B AndradeMultinational Organization Network Sponsoring Translational and Epidemiological Research Initiative, Salvador, BA, Brasil.
Timothy R SterlingVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.
Valeria C RollaFundação Oswaldo Cruz-Fiocruz, Instituto Nacional de Infectologia Evandro Chagas, Rio de Janeiro, RJ, Brasil.
Regional Prospective Observational Research in Tuberculosis (RePORT)-Brazil Consortium
Aline BenjaminFundação Oswaldo Cruz-Fiocruz, Instituto Nacional de Infectologia Evandro Chagas, Rio de Janeiro, RJ, Brasil.
Flavia M Sant'AnnaFundação Oswaldo Cruz-Fiocruz, Instituto Nacional de Infectologia Evandro Chagas, Rio de Janeiro, RJ, Brasil.
Jamile Garcia de OliveiraClínica de Saúde Rinaldo Delamare, Rio de Janeiro, RJ, Brasil.
João MarinClínica de Saúde Rinaldo Delamare, Rio de Janeiro, RJ, Brasil.
Adriana RezendeSecretaria de Saúde de Duque de Caxias, Rio de Janeiro, RJ, Brasil.
Anna Cristina CarvalhoSecretaria de Saúde de Duque de Caxias, Rio de Janeiro, RJ, Brasil.
Michael RochaInstituto Brasileiro para Investigação da Tuberculose, Fundação José Silveira, Salvador, BA, Brasil.
Betânia NogueiraInstituto Brasileiro para Investigação da Tuberculose, Fundação José Silveira, Salvador, BA, Brasil.
Alexandra BritoFundação Medicina Tropical Dr Heitor Vieira Dourado, Manaus, AM, Brasil.
Renata SpenerFundação Medicina Tropical Dr Heitor Vieira Dourado, Manaus, AM, Brasil.
Megan TurnerVanderbilt University Medical Center, Department of Medicine, Division of Infectious Diseases, Nashville, TN, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTuberculosis/human immunodeficiency virus (TB/HIV) coinfection is associated with advanced HIV disease and variable responses to antiretroviral therapy (ART).

objectivesWe examined whether baseline HIV severity markers, ART regimes, or human genetic variants influenced HIV-1 virologic suppression in HIV-associated TB.

methodsWe included TB/HIV participants from Regional Prospective Observational Research in Tuberculosis (RePORT)-Brazil study, who received standard TB therapy and antiretroviral treatment. The primary endpoint was HIV-1 virologic suppression (≤ 1,000 copies/mL); Baseline characteristics, viral load (VL), CD4 cell count, timing of ART initiation, and ART regimens were included. We genotyped UGT1A1 (rs887829; integrase strand transfer inhibitor-related) and CYP2B6 [rs3745274, rs28399499, rs4803419; efavirenz (EFZ)-related]; all have defined normal, intermediate, and slow genotypes. Genotyping was performed by MassARRAY iPLEX Gold; Kaplan-Meier curves compared time-to-suppression with log-rank tests; Cox proportional hazards models estimated hazard ratios.

findingsAmong 194 participants, 68% (n = 132) achieved virologic suppression (≤ 1,000 copies/mL). Median time-to-suppression: 84 days [95% confidence interval (CI): 42-125]. Participants with higher baseline viral load (BVL) (≥ 5 log10 copies/mL) had delayed suppression compared with those with lower VL (< 5 log10; log-rank χ² = 75.9; p < 0.001). Individuals with CD4 ≤ 200 cells/µL suppressed more slowly than those with CD4 > 200 cells/µL (log-rank χ² = 29.6; p < 0.001). Participants starting ART before TB treatment achieved suppression faster than ART-naïve individuals (32 vs. 147 days; log-rank χ² = 48.5; p < 0.001). Higher BVL was associated with reduced hazard of suppression [adjusted hazard ratio (aHR) = 0.67; 95% CI: 0.61-0.75], while higher baseline CD4 count increased the hazard of suppression (per 100 cells/µL: aHR = 1.11; 95% CI: 1.01-1.21). ART-naïve status was associated with lower hazard of suppression in univariate analysis (Hazard Ratio = 0.51; 95% CI: 0.36-0.72) but not after adjustment. ART regimen class and pharmacogenetic metabolizer profiles were not significantly associated with virologic suppression. MAIN

conclusionsBVL and CD4 count were the strongest determinants of virologic suppression in TB/HIV patients. Suppression rates were low, and neither ART regimen nor pharmacogenetic profiles significantly influenced the likelihood of suppression.

Indexed as

AIDS-Related Opportunistic InfectionsAnti-HIV AgentsHIV-1HIV InfectionsTuberculosisAdultBrazilCD4 Lymphocyte CountCoinfectionFemaleGenotypeGlucuronosyltransferaseHumansMaleProspective StudiesTreatment OutcomeAnti-HIV AgentsGlucuronosyltransferaseUGT1A1 Enzyme

Identifiers

PMID42454801
PMCPMC13336628

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.