Evidence map›Paper›PMID 27932622›Full record

Observational studyThe Journal of infectious diseases2017

Inflammasome Activation Underlying Central Nervous System Deterioration in HIV-Associated Tuberculosis.

Suzaan Marais, Rachel P J Lai, Katalin A Wilkinson, Graeme Meintjes, Anne O'Garra, Robert J Wilkinson

Open access · hybridAbstract readObservational Study
In one paragraph

Observational study in The Journal of infectious diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
10.0field-weighted citation impact, top 1% 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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  15. Paradoxical manifestations during tuberculous meningitis treatment among HIV-negative patients: a retrospective descriptive study and literature review.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 4 countries.

Suzaan MaraisClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Rachel P J LaiClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Katalin A WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Graeme MeintjesClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Anne O'GarraLaboratory of Immuno regulation and Infection, The Francis Crick Institute, London, UK.
Robert J WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Observatory 7925, South Africa.
Wellcome Centre for Infectious Diseases Research in Africa · ZAImperial College London · GBNational Tuberculosis Institute · INThe Francis Crick Institute · GBUniversity of Cape Town · ZA

Funding

Medical Research Council MC_U117565642
6 · The paper itself

Abstract

Tuberculous meningitis (TBM) is a frequent cause of meningitis in individuals with human immunodeficiency virus (HIV) infection, resulting in death in approximately 40% of affected patients. A severe complication of antiretroviral therapy (ART) in these patients is neurological tuberculosis-immune reconstitution inflammatory syndrome (IRIS), but its underlying cause remains poorly understood. To investigate the pathogenesis of TBM-IRIS, we performed longitudinal whole-blood microarray analysis of HIV-infected patients with TBM and reflected the findings at the protein level. Patients in whom TBM-IRIS eventually developed had significantly more abundant neutrophil-associated transcripts, from before development of TBM-IRIS through IRIS symptom onset. After ART initiation, a significantly higher abundance of transcripts associated with canonical and noncanonical inflammasomes was detected in patients with TBM-IRIS than in non-IRIS controls. Whole-blood transcriptome findings complement protein measurement from the site of disease, which together suggest a dominant role for the innate immune system in the pathogenesis of TBM-IRIS.

Indexed as

AdultAntiretroviral Therapy, Highly ActiveCaspase 1Caspase 3Caspases, InitiatorCentral Nervous SystemComplement System ProteinsFemaleHIV InfectionsHumansImmune Reconstitution Inflammatory SyndromeInflammasomesLymphocyte CountMaleMiddle AgedNeutrophilsCASP3 protein, humanCASP4 protein, humanCaspase 1Caspase 3Caspases, InitiatorComplement System ProteinsInflammasomesHIVinflammasomesmicroarrayneutrophilsTuberculosis meningitis

Identifiers

PMID27932622
PMCPMC5388298
OpenAlexW2560361100

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.