Evidence map›Paper›PMID 30283448›Full record

ReviewFrontiers in immunology2018

The Pathogenesis of Tuberculosis: The Early Infiltrate of Post-primary (Adult Pulmonary) Tuberculosis: A Distinct Disease Entity.

Robert L Hunter

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Circulating antibody signatures againstFrontiers in immunology · 2026
    Article
  7. An overview on central nervous system tuberculosis (CNS-TB) focusing on cognitive impairments.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Journal of clinical tuberculosis and other mycobacterial diseases · 2024
    Review
  19. Review
  20. Review

1 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, The University of Texas Health Science Center at Houston, Houston, TX, United States.
The University of Texas Health Science Center at Houston · US

Funding

Molecular Basis of Infectious Diseases Training GrantT32AI055449 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI LORENZ, MICHAEL C · 2005 to 2025
$2.6M
Genetic Control of Pulmonary Cavities in TuberculosisR01HL068537 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HUNTER, ROBERT L. · 2001 to 2005
$2.2M
NHLBI NIH HHS R01 HL068537NIAID NIH HHS T32 AI055449
6 · The paper itself

Abstract

It has long been recognized that tuberculosis (TB) induces both protective and tissue damaging immune responses. This paper reviews nearly two centuries of evidence that protection and tissue damage are mediated by separate disease entities in humans. Primary TB mediates protective immunity to disseminated infection while post-primary TB causes tissue damage that results in formation of cavities. Both are necessary for continued survival of Mycobacterium tuberculosis (MTB). Primary TB has been extensively studied in humans and animals. Post-primary TB, in contrast, is seldom recognized or studied. It begins as an asymptomatic early infiltrate that may resolve or progress by bronchogenic spread to caseous pneumonia that either fragments to produce cavities or is retained to produce post-primary granulomas and fibrocaseous disease. Primary and post-primary TB differ in typical age of onset, histopathology, organ distribution, x-ray appearance, genetic predisposition, immune status of the host, clinical course and susceptibility to protection by BCG. MTB is a highly successful human parasite because it produces both primary and post-primary TB as distinct disease entities in humans. No animal reproduces this sequence of lesions. Recognition of these facts immediately suggests plausible solutions, animal models and testable hypotheses to otherwise inaccessible questions of the immunity and pathogenesis of TB.

Indexed as

Adaptive ImmunityAnimalsHost-Pathogen InteractionsHumansMycobacterium tuberculosisTime FactorsTuberculosisTuberculosis, PulmonaryVirulencehumanlungpathogenesispathologypost-primarytuberculosisx-ray

Identifiers

PMID30283448
PMCPMC6156532
OpenAlexW2890138007

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.