Evidence map›Paper›PMID 19000013›Full record

ArticleThe Journal of infectious diseases2008

Early depletion of Mycobacterium tuberculosis-specific T helper 1 cell responses after HIV-1 infection.

Christof Geldmacher, Alexandra Schuetz, Njabulo Ngwenyama, Joseph P Casazza, Erica Sanga, Elmar Saathoff, Catharina Boehme, Steffen Geis, Leonard Maboko, Mahavir Singh and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

110 citing papers in PubMed, 180 citations in OpenAlex.

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  6. HCV-specific CD4EBioMedicine · 2026
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  18. Host Cell Death and Modulation of Immune Response againstInternational journal of molecular sciences · 2024
    Review
  19. Article
  20. Article

50 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 8 institutions in 4 countries.

Christof GeldmacherImmunology Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. geldmacher@lrz.uni-muenchen.de
Alexandra Schuetz
Njabulo Ngwenyama
Joseph P Casazza
Erica Sanga
Elmar Saathoff
Catharina Boehme
Steffen Geis
Leonard Maboko
Mahavir Singh
Fred Minja
Andreas Meyerhans
Richard A Koup
Michael Hoelscher
Ludwig-Maximilians-Universität München · DENational Institute for Medical Research · TZNational Institutes of Health · USFoundation for Innovative New Diagnostics · CHLionex (Germany) · DEMbeya University of Science and Technology · TZNational Institute of Allergy and Infectious Diseases · USSaarland University · DE

Funding

HIV/SIV Replication In VivoZIAAI005014 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI KOUP, RICHARD A · 2009 to 2025
$22.7M
Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

backgroundThe acid-fast bacillus Mycobacterium tuberculosis is often the first manifestation of acquired immunodeficiency syndrome in patients infected with human immunodeficiency virus (HIV). This study was conducted to better understand the mechanism underlying M. tuberculosis-specific pathogenicity early after onset of HIV infection.

methodsM. tuberculosis-specific T helper 1 (Th1) cells were studied in HIV negative (n=114) and chronically HIV infected (n=68) Tanzanian subjects by using early secreted antigenic target 6 (ESAT6) protein or tuberculin (purified protein derivative) with interferon-gamma ELISPOT and intracellular cytokine staining. In a longitudinal study, the effect of acute HIV infection on M. tuberculosis-specific Th1 cells was determined by polychromatic flow cytometric analysis in 5 subjects with latent M. tuberculosis infection who became infected with HIV.

resultsIn tuberculosis (TB)-asymptomatic subjects (i.e., subjects with unknown TB status who did not show clinical signs suggestive of TB), chronic HIV infection was associated with a decreased percentage of subjects with detectable M. tuberculosis-specific Th1 cells (P< .001) a decrease which was not observed among subjects with active TB. Acute HIV infection induced a rapid depletion of M. tuberculosis-specific Th1 cells in 4 subjects remained TB asymptomatic, whereas the population of these cells remained stable in subjects who remained HIV negative (P< .01).

conclusionsTaken together, these data suggest a mechanism of rapid M. tuberculosis-specific Th1 cell depletion that may contribute to the early onset of TB in individuals with latent M. tuberculosis infection who become HIV infected.

Indexed as

Antigens, BacterialBacterial ProteinsCD4-Positive T-LymphocytesCross-Sectional StudiesGene Expression RegulationHIV InfectionsHumansMycobacterium tuberculosisReceptors, CCR5Th1 CellsTuberculosisAntigens, BacterialBacterial ProteinsESAT-6 protein, Mycobacterium tuberculosisReceptors, CCR5

Identifiers

PMID19000013
PMCPMC2650495
OpenAlexW2166696946

What OpenQuestion holds

Textmetadata
LicenceTDM
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.