Evidence map›Paper›PMID 26051653›Full record

Observational studyTuberculosis (Edinburgh, Scotland)2015

Kinetics of Mycobacterium tuberculosis-specific IFN-γ responses and sputum bacillary clearance in HIV-infected adults during treatment of pulmonary tuberculosis.

David T Mzinza, Derek J Sloan, Kondwani C Jambo, Doris Shani, Mercy Kamdolozi, Katalin A Wilkinson, Robert J Wilkinson, Geraint R Davies, Robert S Heyderman, Henry C Mwandumba

Open access · hybridAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in Tuberculosis (Edinburgh, Scotland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 93% of its field
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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. T cell responses toVaccine: X · 2022
    Article
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

10 authors at 2 institutions in 3 countries.

David T MzinzaMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi. Electronic address: dmzinza@gmail.com.
Derek J SloanMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi; Department of Medicine, College of Medicine, Private Bag 360, Chichiri, Blantyre 3, Malawi; Institute of Infection and Global Health, University of Liverpool, Liverpool L6 1LY, UK. Electronic address: Derek.Sloan@lstmed.ac.uk.
Kondwani C JamboMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi; Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool L3 5QA, UK. Electronic address: Kjambo@liverpool.ac.uk.
Doris ShaniMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi. Electronic address: dshani@mlw.medcol.mw.
Mercy KamdoloziMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi. Electronic address: mkamdolozi@mlw.medcol.mw.
Katalin A WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Rondebosch 7701, Cape Town, South Africa; MRC National Institute for Medical Research, London NW7 1AA, UK. Electronic address: Katalin.Wilkinson@uct.ac.za.
Robert J WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Rondebosch 7701, Cape Town, South Africa; MRC National Institute for Medical Research, London NW7 1AA, UK; Department of Medicine, Imperial College, London SW7 2AZ, UK. Electronic address: Robert.Wilkinson@uct.ac.za.
Geraint R DaviesMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi; Department of Medicine, College of Medicine, Private Bag 360, Chichiri, Blantyre 3, Malawi; Institute of Infection and Global Health, University of Liverpool, Liverpool L6 1LY, UK. Electronic address: gerrydavies@doctors.org.uk.
Robert S HeydermanMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi; Department of Medicine, College of Medicine, Private Bag 360, Chichiri, Blantyre 3, Malawi; Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool L3 5QA, UK. Electronic address: livrsh@liverpool.ac.uk.
Henry C MwandumbaMalawi-Liverpool-Wellcome Trust Clinical Research Programme, University of Malawi College of Medicine, P.O. Box 30096, Chichiri, Blantyre 3, Malawi; Department of Medicine, College of Medicine, Private Bag 360, Chichiri, Blantyre 3, Malawi; Department of Clinical Sciences, Liverpool School of Tropical Medicine, Liverpool L3 5QA, UK. Electronic address: Henry.Mwandumba@lstmed.ac.uk.
University of Liverpool · GBUniversity of Cape Town · ZA

Funding

Wellcome Trust 100890Wellcome Trust 104803
6 · The paper itself

Abstract

In HIV-uninfected adults with pulmonary tuberculosis (TB), anti-TB treatment is associated with changes in Mycobacterium tuberculosis (Mtb)-specific immune responses, which correlate with sputum bacillary load. It is unclear if this occurs in HIV-infected TB patients. We investigated changes in Mtb-specific immune responses and sputum bacillary clearance during anti-TB treatment in HIV-infected and HIV-uninfected adults with pulmonary TB. Sputum bacillary load was assessed by smear microscopy and culture. Mtb-specific IFN-γ secreting peripheral blood mononuclear cells were enumerated using an ELISPOT assay following stimulation with PPD, ESAT-6 and CFP-10. The baseline frequency of Mtb-specific IFN-γ secreting cells was lower in HIV-infected than HIV-uninfected patients (median PPD 32 vs. 104 Spot Forming Units (SFU), p = 0.05; CFP-10 19 vs. 74 SFU, p = 0.01). ESAT-6-specific IFN-γ secreting cells and sputum bacillary load declined progressively during treatment in both HIV-infected and HIV-uninfected patients. HIV infection did not influence the 2-month sputum culture conversion rate (Odds Ratio 0.89, p = 0.95). These findings suggest that changes in ESAT-6-specific immune responses during anti-TB treatment correspond with changes in sputum bacillary load irrespective of host HIV infection status. The utility of Mtb-specific IFN-γ responses as a proxy measure of treatment response in HIV-infected TB patients warrants further evaluation in other settings.

Indexed as

CoinfectionAdultAntitubercular AgentsBacterial LoadCells, CulturedEnzyme-Linked Immunospot AssayFemaleHIV InfectionsHost-Pathogen InteractionsHumansInterferon-gammaInterferon-gamma Release TestsKineticsLeukocytes, MononuclearLinear ModelsLogistic ModelsAntitubercular AgentsIFNG protein, humanInterferon-gammaAntigen-specific immunityAnti-tuberculosis treatmentHIV infectionIFN-γMycobacterium tuberculosisPulmonary tuberculosis

Identifiers

PMID26051653
PMCPMC4503815
OpenAlexW2142346689

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.