CoChat
Sign Up
Cited by 208Viral Infections and Immunology ResearchCardiac Fibrosis and RemodelingImmunotoxicology and immune responses

Coxsackievirus-induced myocarditis in mice: A model of autoimmune disease for studying immunotoxicity

Open access
Fairweather, DeLisa, Rose, Noel R.·2007·Methods
DOI 10.1016/j.ymeth.2006.07.009PMC PMC1764911
Open this paper in CoChat — free account

Abstract

Excellent animal models are available for virus-induced and autoimmune heart disease that are remarkably similar to human disease. Developing good animal models for heart disease is crucial because cardiovascular disease is now the leading cause of death in the United States and is estimated to be the leading cause of death in the world by the year 2020. A significant proportion of heart disease in Western populations is associated with inflammation. Myocarditis, or inflammation of the heart muscle, is the major cause of sudden death in young adults. Although most individuals recover from acute myocarditis, genetically susceptible individuals may go on to develop chronic myocarditis and dilated cardiomyopathy (DCM) resulting in congestive heart failure. In this article, we describe a model of autoimmune myocarditis and DCM induced by inoculation with heart-passaged coxsackievirus B3 (CVB3). Intraperitoneal inoculation of susceptible mice with CVB3 induces acute cardiac inflammation from days 7 to 14 postinfection (pi) that progresses to chronic myocarditis and DCM from day 28 to at least 56 pi. The model of CVB3-induced myocarditis presented here allows dissection of the contribution of viral infection and xenobiotics on immune dysregulation and inflammation in the heart. An improved understanding of the interaction between environmental exposures and the development of heart disease represents a clear challenge for immunotoxicologists.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.ymeth.2006.07.009

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Male mice develop more consistent and severe EAM than females, exhibiting stronger pro-inflammatory macrophage responses, greater cardiac infiltration, and more pronounced fibrotic remodelling.

    “This was a deliberate experimental decision, as male mice develop more consistent and severe EAM than females, exhibiting stronger pro-inflammatory macrophage responses, greater cardiac infiltration, and more pronounced fibrotic remodelling, which are features that are well-documented in both autoimmune and viral myocarditis models and align with the higher incidence and severity of myocarditis”

    From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [34]

    The Introduction reports that young male BALB/c mice develop significantly greater acute and chronic myocarditis than females after CVB3 infection. It describes macrophage-rich infiltration and later fibrosis in that viral model, but does not establish greater consistency or stronger pro-inflammatory macrophage responses, cardiac infiltration, or fibrotic remodelling in males than females. It also does not make the sex comparison for adjuvant-induced EAM specifically. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Mice can develop autoimmune inflammation in the heart even after viral clearance in a coxsackievirus B3-induced myocarditis model.

    “mice can develop autoimmune inflammation in the heart even after viral clearance”

    From Autoimmune Myocarditis, Old Dogs and New Tricks. (2024) · cites this paper as [20]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Research works printed but not linked: 26

  1. [2]Willerson JT, Ridker PM. Circulation. 2004;109(suppl II):II2–II10. doi: 10.1161/01.CIR.0000129535.04194.38. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  2. [3]Dec GW. In: Myocarditis: From Bench to Bedside. Cooper LT Jr, editor. Humana Press; Totowa, New Jersey: 2003. pp. 157–281. [Google Scholar]
  3. [4]Yusuf S, Reddy S, Ounpuu S, Anand S. Circulation. 2001;104:2746–2753. doi: 10.1161/hc4601.099487. [DOI] [PubMed] [Google Scholar] · DOI
  4. [5]Rose NR, Wolfgram LJ, Herkowitz A, Beisel KW. Ann NY Acad Sci. 1986;475:146–156. doi: 10.1111/j.1749-6632.1986.tb20864.x. [DOI] [PubMed] [Google Scholar] · DOI
  5. [7]Fairweather D, Rose NR. Drug Discov Today: Dis Models. 2004;1:381–386. [Google Scholar]
  6. [8]Huber SA, Gauntt CJ, Sakkinen P. Adv Virus Res. 1998;51:35–80. doi: 10.1016/s0065-3527(08)60783-6. [DOI] [PubMed] [Google Scholar] · DOI
  7. [9]Horwitz MS, La Cava A, Fine C, Rodriguez E, Ilic A, Sarvetnick N. Nat Med. 2000;6:693–697. doi: 10.1038/76277. [DOI] [PubMed] [Google Scholar] · DOI
  8. [10]Fong IW. In: Infections and the Cardiovascular System: New perspectives. Fong IW, editor. Kluwer Academic: Plenum Publishers; New York: 2003. pp. 3–31. [Google Scholar]
  9. [11]Fuse K, Chan G, Liu Y, Gudgeon P, Husain M, Chen M, Yeh WC, Akira S, Liu PP. Circulation. 2005;112:2276–2285. doi: 10.1161/CIRCULATIONAHA.105.536433. [DOI] [PubMed] [Google Scholar] · DOI
  10. [12]Neu N, Rose NR, Beisel KW, Herskowitz A, Gurri-Glass G, Craig SW. J Immunol. 1987;139:3630–3636. [PubMed] [Google Scholar]
  11. [13]Fairweather D, Frisancho-Kiss S, Rose NR. Rev Med Virol. 2005;15:17–27. doi: 10.1002/rmv.445. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  12. [14]Fairweather D, Rose NR. Lupus. 2005;14:646–651. doi: 10.1191/0961203305lu2192oa. [DOI] [PubMed] [Google Scholar] · DOI
  13. [15]Fairweather D, Frisancho-Kiss S, Yusung SA, Barrett MA, Gatewood SJL, Davis SE, Njoku DB, Rose NR. Am J Pathol. 2004;165:1883–1894. doi: 10.1016/s0002-9440(10)63241-5. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI · Paper page
  14. [16]Afanasyeva M, Georgakopoulos D, Fairweather D, Caturegli P, Kass DA, Rose NR. 2004 Circulation. 2004;110:2910–2917. doi: 10.1161/01.CIR.0000147538.92263.3A. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  15. [19]Fairweather D, Frisancho-Kiss S, Yusung SA, Barrett MA, Davis SE, Steele RA, Gatewood SJL, Rose NR. J Immunol. 2005;174:261–269. doi: 10.4049/jimmunol.174.1.261. [DOI] [PubMed] [Google Scholar] · DOI · Paper page
  16. [20]Neu N, Beisel KW, Traystman MD, Rose NR. SW Craig J Immunol. 1987;138:2488–2492. [PubMed] [Google Scholar]
  17. [23]Rose NR. Sem Liver Dis. 2002;22:387–394. doi: 10.1055/s-2002-35708. [DOI] [PubMed] [Google Scholar] · DOI
  18. [24]Davidson A, Diamond B. N Engl J Med. 2001;345:340–350. doi: 10.1056/NEJM200108023450506. [DOI] [PubMed] [Google Scholar] · DOI
  19. [25]Brix TH, Kyvik KO, Christensen K, Hegedus L. J Clin Endocrinol Metab. 2001;86:930–934. doi: 10.1210/jcem.86.2.7242. [DOI] [PubMed] [Google Scholar] · DOI
  20. [26]Fairweather D, Rose NR. Emerg Inf Dis. 2004;10:2005–2011. doi: 10.3201/eid1011.040367. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  21. [27]Brook RD, Franklin B, Cascio W, Hong Y, Howard G, Lipsett M, Luepker R, Mittleman M, Samet J, Smith SC, Jr, Tager I. Circulation. 2004;109:2655–2671. doi: 10.1161/01.CIR.0000128587.30041.C8. [DOI] [PubMed] [Google Scholar] · DOI
  22. [28]Doria A, Sarzi-Puttini P. Lupus. 2005;14:643–645. doi: 10.1191/0961203305lu2191ed. [DOI] [PubMed] [Google Scholar] · DOI
  23. [29]Liu PY, Death AK, Handelsman DJ. Endocrine Rev. 2003;24:313–340. doi: 10.1210/er.2003-0005. [DOI] [PubMed] [Google Scholar] · DOI
  24. [30]Huber SA, Pfaeffle B. J Virol. 1994;68:5126–5132. doi: 10.1128/jvi.68.8.5126-5132.1994. [DOI] [PMC free article] [PubMed] [Google Scholar] · DOI
  25. [31]Silbergeld EK, Silva IA, Nyland JF. Toxicol Appl Pharm. 2005;207:S282–S292. doi: 10.1016/j.taap.2004.11.035. [DOI] [PubMed] [Google Scholar] · DOI
  26. [32]Cihakova D, Sharma R, Fairweather D, Afanasyeva M, Rose NR. Methods Mol Med. 2004;102:175–194. doi: 10.1385/1-59259-805-6:175. [DOI] [PubMed] [Google Scholar] · DOI

Cited by

Sorted by citations

Authors
Fairweather, D., & Rose, N. R.
Affiliations
Johns Hopkins University (US)
Corresponding author
Rose, Noel R.
ORCID
Fairweather, DeLisa
Venue
Methods
Publisher
Elsevier BV
Published
2007-01
Volume
41
Issue
1
Pages
118-122
ISSN
1046-2023 (ISSN-L)
DOI
10.1016/j.ymeth.2006.07.009
PMC
PMC1764911
OpenAlex
W1980444116
Cited by
208
References
5
Citations by year
2026: 12 · 2025: 12 · 2024: 13 · 2023: 14 · 2022: 11 · 2021: 10 · 2020: 15 · 2019: 9 · 2018: 6 · 2017: 13 · 2016: 7 · 2015: 5 · 2014: 10 · 2013: 10 · 2012: 20
FWCI
6.19
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Methods (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (HL 67290, R01HL077611, R01HL067290, HL 70729, R01HL070729)
  • National Institute of Allergy and Infectious Diseases (AI 51835, R21AI051835)
  • National Institute of Environmental Health Sciences (ES03819, P30ES003819)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords
coxsackievirus B3, myocarditis, dilated cardiomyopathy, autoimmune heart disease, immunotoxicity, animal models, viral infection, cardiac inflammation, immune dysregulation, xenobiotics, environmental exposure
MeSH terms
Animals, Autoimmune Diseases, Chlorocebus aethiops, Coxsackievirus Infections, Disease Models, Animal, Flow Cytometry, Injections, Intraperitoneal, Mice, Inbred BALB C, Myocarditis, Vero Cells, Xenobiotics, Enterovirus B, Human, Mice

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review