Evidence map›Paper›PMID 26980490›Full record

ReviewTuberculosis (Edinburgh, Scotland)2016

Tuberculosis as a three-act play: A new paradigm for the pathogenesis of pulmonary tuberculosis.

Robert L Hunter

Open access · hybridAbstract readReview
In one paragraph

Review in Tuberculosis (Edinburgh, Scotland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 1 pooled it
13.2field-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

98 citing papers in PubMed, 1 synthesis or guideline pooled it, 195 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Biofilm Associated Persistence and Drug Tolerance in Mycobacteria Within Host Microenvironments.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026
    Review
  5. Review
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  7. Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026
    Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
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  19. Review
  20. Article

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

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

1 author at 1 institution in 1 country.

Robert L HunterDepartment of Pathology and Laboratory Medicine, University of Texas Health Sciences Center at Houston, MSB 2.136, 6431 Fannin, Houston, TX 77030, USA. Electronic address: Robert.L.Hunter@uth.tmc.edu.
The University of Texas Health Science Center · US

Funding

Genetic Control of Pulmonary Cavities in TuberculosisR01HL068537 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HUNTER, ROBERT L. · 2001 to 2005
$2.2M
Mechanisms of Mycobacterial Antigen ProcessingR01AI078420 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI JAGANNATH, CHINNASWAMY · 2009 to 2013
$2.2M
NHLBI NIH HHS HL068537NHLBI NIH HHS R01 HL068537NIAID NIH HHS AI078420NIAID NIH HHS R01 AI078420
6 · The paper itself

Abstract

Lack of access to human tissues with untreated tuberculosis (TB) has forced generations of researchers to use animal models and to adopt a paradigm that granulomas are the characteristic lesion of both primary and post primary TB. An extended search of studies of human lung tissues failed to find any reports that support this paradigm. We found scores of publications from gross pathology in 1804 through high resolution CT scans in 2015 that identify obstructive lobular pneumonia, not granulomas, as the characteristic lesion of developing post-primary TB. This paper reviews this literature together with other relevant observations to formulate a new paradigm of TB with three distinct stages: a three-act play. First, primary TB, a war of attrition, begins with infection that spreads via lymphatics and blood stream before inducing systemic immunity that contains and controls the organisms within granulomas. Second, post-primary TB, a sneak attack, develops during latent TB as an asymptomatic obstructive lobular pneumonia in persons with effective systemic immunity. It is a paucibacillary process with no granulomas that spreads via bronchi and accumulates mycobacterial antigens and host lipids for 1-2 years before suddenly undergoing caseous necrosis. Third, the fallout, is responsible for nearly all clinical post primary disease. It begins with caseous necrotic pneumonia that is either retained to become the focus of fibrocaseous disease or is coughed out to leave a cavity. This three-stage paradigm suggests testable hypotheses and plausible answers to long standing questions of immunity to TB.

Indexed as

AnimalsAntigens, BacterialDisease ProgressionEpitopes, T-LymphocyteGranulomaHost-Pathogen InteractionsHumansLatent TuberculosisLungMycobacterium tuberculosisTuberculosis, PulmonaryAntigens, BacterialEpitopes, T-LymphocyteCavityHumanLungPathogenesisPathologyPost primary

Identifiers

PMID26980490
PMCPMC4795183
OpenAlexW2229191546

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.