Evidence map›Paper›PMID 19014757›Full record

ReviewThe Journal of allergy and clinical immunology2008

Host immune responses to rhinovirus: mechanisms in asthma.

John T Kelly, William W Busse

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 107 citations in OpenAlex.

  1. Effects of montelukast on patients with asthma after experimental inoculation with human rhinovirus 16.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2011
    Trial
  2. Allergic sensitization is associated with rhinovirus-, but not other virus-, induced wheezing in children.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2010
    Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Non-typeableEuropean respiratory review : an official journal of the European Respiratory Society · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Azithromycin in viral infections.Reviews in medical virology · 2021
    Review
  16. Observational
  17. Review
  18. Article
  19. Article
  20. Article
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.

John T KellySection of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wis.
William W BusseSection of Allergy, Pulmonary and Critical Care Medicine, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, Wis. Electronic address: wwb@medicine.wisc.edu.
University of Wisconsin–Madison · US

Funding

Severe Asthma From Respiratory InfectionsR01HL069116 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI BUSSE, WILLIAM W. · 2001 to 2010
$7.6M
Wisconsin Allergy Research Training (WISCART) ProgramT32AI007635 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI James E. Gern, DANIEL J JACKSON · 2000 to 2026
$6.5M
NHLBI NIH HHS HL069116NHLBI NIH HHS R01 HL069116NIAID NIH HHS T32 AI007635
6 · The paper itself

Abstract

Viral respiratory infections can have a profound effect on many aspects of asthma including its inception, exacerbations, and, possibly, severity. Of the many viral respiratory infections that influence asthma, the common cold virus, rhinovirus, has emerged as the most frequent illness associated with exacerbations and other aspects of asthma. The mechanisms by which rhinovirus influences asthma are not fully established, but current evidence indicates that the immune response to this virus is critical in this process. Many airway cell types are involved in the immune response to rhinovirus, but most important are respiratory epithelial cells and possibly macrophages. Infection of epithelial cells generates a variety of proinflammatory mediators to attract inflammatory cells to the airway with a subsequent worsening of underlying disease. Furthermore, there is evidence that the epithelial airway antiviral response to rhinovirus may be defective in asthma. Therefore, understanding the immune response to rhinovirus is a key step in defining mechanisms of asthma, exacerbations, and, perhaps most importantly, improved treatment.

Indexed as

AsthmaCell MovementEpithelial CellsHumansImmunity, CellularInflammation MediatorsMacrophagesPicornaviridae InfectionsRespiratory Tract InfectionsRhinovirusInflammation Mediators

Identifiers

PMID19014757
PMCPMC3927944
OpenAlexW2003779030

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.