Evidence map›Paper›PMID 22488075›Full record

ReviewCurrent opinion in rheumatology2012

Update on coxsackievirus B3 myocarditis.

DeLisa Fairweather, Katelyn A Stafford, Yoon K Sung

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

86 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Tnni3k Is Cardioprotective in Viral Myocarditis.Journal of cardiovascular development and disease · 2026
    Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. T-Cell Receptor Sequences Identify Combined Coxsackievirus-International journal of molecular sciences · 2024
    Article
  20. Article

26 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

3 authors at 1 institution in 1 country.

DeLisa FairweatherDepartment of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, USA. dfairwea@jhsph.edu
Katelyn A Stafford
Yoon K Sung
Johns Hopkins University · US

Funding

Traning Program in Environmental Health SciencesT32ES007141 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI Marsha Wills-Karp · 1985 to 2026
$22.2M
Regulating heart disease: the adjuvant effect of viral infection.R01HL087033 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI FAIRWEATHER, DELISA · 2007 to 2011
$2.5M
Sex Differences in Complement during Myocarditis/DCMR01HL111938 · NHLBI · MAYO CLINIC JACKSONVILLE · PI FAIRWEATHER, DELISA · 2012 to 2015
$1.6M
NHLBI NIH HHS R01 HL087033NHLBI NIH HHS R01 HL111938NIEHS NIH HHS T32 ES007141
6 · The paper itself

Abstract

purpose of reviewTo present recent findings on the pathogenesis of coxsackievirus B3 (CVB3) myocarditis based on animal models, with a focus on the role of T helper (Th) immune responses in disease progression. RECENT

findingsAcute CVB3 myocarditis is known to be increased by Th1 immune responses, but recent findings indicate that Th1-type immunity protects against acute myocarditis by reducing viral replication and prevents the progression to chronic myocarditis and dilated cardiomyopathy (DCM) by inhibiting Th2 responses. Th2 responses reduce acute myocarditis by inhibiting Th1 responses via regulatory T cells and anti-inflammatory cytokines, but can be deleterious when they induce acute cardiac remodeling leading to chronic myocarditis/DCM. Th2-skewed immune responses allow resistant strains of mice to progress from myocarditis to DCM. In contrast, Th17 responses are elevated during acute and chronic myocarditis and have been found to contribute to cardiac remodeling and DCM. SUMMARY: Recent data indicate that elevated Th2 and Th17 responses during acute CVB3 myocarditis are critical for the progression from myocarditis to DCM and heart failure because of their ability to induce cardiac remodeling. Th1 responses protect against CVB3 myocarditis by inhibiting Th2 responses and viral replication, but increase acute inflammation.

Indexed as

Enterovirus B, HumanAnimalsAutoimmune DiseasesCoxsackievirus InfectionsDisease Models, AnimalMiceMyocarditisT-Lymphocytes, Helper-Inducer

Identifiers

PMID22488075
PMCPMC4536812
OpenAlexW2312220900

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.