Evidence map›Paper›PMID 26595738›Full record

ReviewAnnals of the American Thoracic Society2015

Viruses in Idiopathic Pulmonary Fibrosis. Etiology and Exacerbation.

Bethany B Moore, Thomas A Moore

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 3 pooled it
7.4field-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

69 citing papers in PubMed, 3 syntheses or guidelines pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Proteomic Approach to Study the Effect ofJournal of fungi (Basel, Switzerland) · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Persistent microbial infections and idiopathic pulmonary fibrosis - an insight intoFrontiers in cellular and infection microbiology · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. Article

9 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

2 authors at 1 institution in 1 country.

Bethany B Moore1 Department of Internal Medicine and.
Thomas A Moore1 Department of Internal Medicine and.
University of Michigan · US

Funding

miR-29b and autophagy regulate alveolar macrophage function post-BMTR01AI117229 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2015 to 2019
$2.2M
Periostin Regulation of Lung FibrosisR01HL115618 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2013 to 2016
$1.6M
HSCT-induced alterations in DCs to promote IL-17 and lung pathologyR01HL127805 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MOORE, BETHANY B. · 2016 to 2018
$1.5M
NHLBI NIH HHS HL115618NHLBI NIH HHS R01 HL115618NHLBI NIH HHS R01 HL127805NIAID NIH HHS AI117229NIAID NIH HHS R01 AI117229
6 · The paper itself

Abstract

Viral infections are important contributors to exacerbation of asthma and chronic obstructive pulmonary disease; however, the role of viruses in the pathogenesis of idiopathic pulmonary fibrosis (IPF) is less clear. This likely reflects that fact that IPF acute exacerbations are defined clinically as "noninfectious," and little attention has been paid to the outcomes of patients with IPF with diagnosed infections. However, accumulating evidence suggests that infections (both bacterial and viral) may influence disease outcomes either as exacerbating agents or initiators of disease. Support for a viral role in disease initiation comes from studies demonstrating the presence of herpesviral DNA and epithelial cell stress in the lungs of asymptomatic relatives at risk for developing familial IPF. In addition, the number of studies that can associate viral (especially herpesviral) signatures in the lung with the development of IPF is steadily growing, and activated leukocyte signatures in patients with IPF provide further support for infectious processes driving IPF progression. Animal modeling has been used to better understand how a gamma herpesvirus infection can modulate the pathogenesis of lung fibrosis and has demonstrated that preceding infections appear to reprogram lung epithelial cells during latency to produce profibrotic factors, making the lung more susceptible to subsequent fibrotic insult, whereas exacerbations of existing fibrosis, or infections in susceptible hosts, involve active viral replication and are influenced by antiviral therapy. In addition, there is new evidence that bacterial burden in the lungs of patients with IPF may predict a poor prognosis.

Indexed as

AgingAcute DiseaseAnimalsBone Marrow TransplantationDisease Models, AnimalDisease ProgressionEpithelial CellsHerpesviridaeHerpesviridae InfectionsHumansIdiopathic Pulmonary FibrosisLungMiceVirus Diseasesagingfibroblastherpesvirusimmunitylung

Identifiers

PMID26595738
PMCPMC4722834
OpenAlexW2176818153

What OpenQuestion holds

Textmetadata
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.