Enteroviral Cardiomyopathy: Bad News for the Dystrophin-Glycoprotein Complex

Badorff, Cornel; Lee, Gil-Hwan; Knowlton, Kirk U.

doi:10.1007/s000590050011

Cited by 29 publications

(14 citation statements)

References 42 publications

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“…The cardiac phenotype of some dystrophin mutations was found to result from an alteration of the promoter region required for specific expression of this protein in cardiomyocytes, or from conformational changes of the dystrophin rod or hinge regions (221). It is worth mentioning that the disruption of the dystrophin complex was also found in viral myocarditis (222,223), which may provide an explanation for the acquired form of DCM.…”

Section: Hypertrophic Cardiomyopathymentioning

confidence: 99%

Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies

Macháčková¹,

Barta²,

Dhalla³

2006

Canadian Journal of Cardiology

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Section: Hypertrophic Cardiomyopathymentioning

confidence: 99%

Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies

Macháčková¹,

Barta²,

Dhalla³

2006

Canadian Journal of Cardiology

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“…Certainly, virus infection directly damages heart cells either by disrupting cardiac function [1,2,39], or directly killing infected myocardial cells [12,20,29]. The ultimate importance of direct virus pathogenicity likely will depend on the extent of infection.…”

Section: Introductionmentioning

confidence: 98%

Increased susceptibility of male BALB/c mice to coxsackievirus B3-induced myocarditis: role for CD1d

Huber

2004

Med Microbiol Immunol

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BALB/c male mice infected with the H3 variant of coxsackievirus B3 (CVB3) develop fulminant myocarditis. Age-matched female mice show little myocarditis due to decreased virus receptor expression on cardiac cells. TNFalpha and IL-1beta levels were increased in males by 3 days after infection. IFNgamma levels increased more slowly throughout the 7-day observation period. CD4+, CD8+, macrophage (Mac3+) and gammadelta+ cells all accumulated in male hearts, with gammadelta+ cells showing early (day 3) infiltration. Females also accumulated CD4+ cells, but few of the other cell types. CD4+ cells in male hearts predominately produced IFNgamma, indicating a Th1 cell phenotype, whereas CD4+ cells in females produced IL-4, but little IFNgamma, indicating a Th2 phenotype. CD1d, a major histocompatibility complex I-like molecule often implicated in innate immunity, was increased in CVB3-infected male but not female cardiocytes both in vivo and in vitro. These results demonstrate that CVB3 infections produce gender-specific differences in both innate and adaptive immunity, which may explain the difference in disease susceptibility.

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“…Dendritic cells in the mice also become infected and affect levels of IL-10, IL-6, and TNF-␣ (36). Other studies with animal models have demonstrated that enteroviral protease 2A cleaves dystrophin, thereby disrupting the integrity of the sarcolemmal dystrophin-glycoprotein complex (37)(38)(39).…”

Section: Discussionmentioning

confidence: 99%

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

et al. 2009

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ABSTRACT:The significance of minor myocardial inflammatory infiltrates and viral detection in SIDS is controversial. We retrospectively compared the demographic profiles, myocardial inflammation, cardiomyocyte necrosis, and myocardial virus detection in infants who died of SIDS in a safe sleep environment, accidental suffocation, or myocarditis. Formalin-fixed, paraffin-embedded myocardial sections were semiquantitatively assessed for CD3 lymphocytes and CD68 macrophages using immunohistochemistry and for cardiomyocyte cell death in H&E-stained sections. Enteroviruses and adenoviruses were searched for using PCR technology. The means of lymphocytes, macrophages, and necrotic cardiomyocytes were not statistically different in SIDS and suffocation cases. Enterovirus, not otherwise specified, was detected in one suffocation case and was the only virus detected in the three groups. Very mild myocardial lymphocyte and macrophage infiltration and scattered necrotic cardiomyocytes in SIDS are not pathologic, but may occur after the developing heart is exposed to environmental pathogens, including viruses. (Pediatr Res 66: 17-21, 2009)

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Enteroviral Cardiomyopathy: Bad News for the Dystrophin-Glycoprotein Complex

Cited by 29 publications

References 42 publications

Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies

Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies

Increased susceptibility of male BALB/c mice to coxsackievirus B3-induced myocarditis: role for CD1d

Myocardial Inflammation, Cellular Death, and Viral Detection in Sudden Infant Death Caused by SIDS, Suffocation, or Myocarditis

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