Evidence map›Paper›PMID 19583510›Full record

ArticleThe Journal of infectious diseases2009

Gene transcript abundance profiles distinguish Kawasaki disease from adenovirus infection.

Stephen J Popper, Virginia E Watson, Chisato Shimizu, John T Kanegaye, Jane C Burns, David A Relman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Gene expression profiles in febrile children with defined viral and bacterial infection.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Trial
  4. Article
  5. Article
  6. Article
  7. Innate immune response analysis in COVID-19 and kawasaki disease reveals MIS-C predictors.Journal of the Formosan Medical Association = Taiwan yi zhi · 2022
    Article
  8. Article
  9. Review
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  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Is Kawasaki disease an infectious disorder?International journal of rheumatic diseases · 2018
    Review
  17. Article
  18. How Should We Classify Kawasaki Disease?Frontiers in immunology · 2018
    Review
  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

6 authors at 4 institutions in 2 countries.

Stephen J PopperDepartment of Microbiology and Immunology, Stanford University School of Medicine, Stanford, , CA 94305, USA. spopper@stanford.edu
Virginia E Watson
Chisato Shimizu
John T Kanegaye
Jane C Burns
David A Relman
Boston Children's Hospital · USUniversity of California, San Diego · USBipar · FRStanford University · US

Funding

Genetic Markers and gene expression in Kawasaki DiseaseR01HL069413 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BURNS, JANE C · 2002 to 2010
$5.5M
NHLBI NIH HHS R01 HL069413NHLBI NIH HHS R01-HL69413
6 · The paper itself

Abstract

backgroundAcute Kawasaki disease (KD) is difficult to distinguish from other illnesses that involve acute rash or fever, in part because the etiologic agent(s) and pathophysiology remain poorly characterized. As a result, diagnosis and critical therapies may be delayed.

methodsWe used DNA microarrays to identify possible diagnostic features of KD. We compared gene expression patterns in the blood of 23 children with acute KD and 18 age-matched febrile children with 3 illnesses that resemble KD.

resultsGenes associated with platelet and neutrophil activation were expressed at higher levels in patients with KD than in patients with acute adenovirus infections or systemic adverse drug reactions, but levels in patients with KD were not higher than those in patients with scarlet fever. Genes associated with B cell activation were also expressed at higher levels in patients with KD than in control subjects. A striking absence of interferon-stimulated gene expression in patients with KD was confirmed in an independent cohort of patients with KD. Using a set of 38 gene transcripts, we successfully predicted the diagnosis for 21 of 23 patients with KD and 7 of 8 patients with adenovirus infection.

conclusionsThese findings provide insight into the molecular features that distinguish KD from other febrile illnesses and support the feasibility of developing novel diagnostic reagents for KD based on the host response.

Indexed as

Gene Expression ProfilingAdenovirus Infections, HumanB-LymphocytesCase-Control StudiesCell AdhesionChildGene Expression RegulationHumansImmunity, InnateInterferonsMucocutaneous Lymph Node SyndromeRNA, ViralInterferonsRNA, Viral

Identifiers

PMID19583510
PMCPMC2878183
OpenAlexW2054384691

What OpenQuestion holds

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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.