Detection of Coxsackie-B-Virus-Specific Rna Sequences in Myocardial Biopsy Samples From Patients With Myocarditis and Dilated Cardiomyopathy

Bowles, Neil E.; Olsen, E. G. J.; Richardson, Peter J.; Archard, L. C.

doi:10.1016/s0140-6736(86)91837-4

Cited by 558 publications

(208 citation statements)

References 14 publications

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“…Persistent enterovirus infection of the myocardium has been reported (Bowles et al, 1986;Kandolf et al, 1987), and the existence of a causative role of enteroviruses in acute myocarditis, particularly in children, finds support in a metaanalysis. On the other hand, some of the studies examining the association of enteroviruses with dilated cardiomyopathy have been negative (Baboonian and Treasure, 1997).…”

mentioning

confidence: 90%

Hepatitis C Virus from the Hearts of Patients with Myocarditis and Cardiomyopathy

Matsumori

Yutani

Ikeda

et al. 2000

Laboratory Investigation

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SUMMARY:The myocardium may be the target of several types of viral infections. The importance of hepatitis C virus (HCV) infection has been recently noted in patients with myocarditis and in patients with dilated or hypertrophic cardiomyopathy. The present study sought to detect HCV genomes in formalin-fixed paraffin sections of autopsied hearts from patients with myocarditis and patients with dilated or hypertrophic cardiomyopathy. Paraffin sections were deparaffinized, RNA was extracted, and the positive and negative strands of HCV RNA were detected by performing reverse transcription and nested polymerase chain reaction. The polymerase chain reaction products were cloned and sequenced. ␤-actin gene was used as a control for the successful amplification of a housekeeping gene. Among 106 hearts examined, ␤-actin gene was amplified in 61 hearts (57.5%). Among the latter, HCV RNA was detected in 13 hearts (21.3%), and negative strands in 4 hearts (6.6%). HCV RNA was found in 4 hearts (33.3%) with myocarditis, in 3 hearts (11.5%) with dilated cardiomyopathy, and in 6 hearts (26.0%) with hypertrophic cardiomyopathy. The sequences recovered from nine patients were highly homologous to the standard strain of HCV. HCV genomes were not found in either 35 hearts from patients with myocardial infarction or 20 hearts from patients with noncardiac diseases. These HCV RNA positive samples were obtained from 1 heart in 1979, 7 hearts between 1980 and 1989, and 5 hearts since 1990, indicating that HCV RNA can be amplified from paraffin-embedded hearts preserved for many years. This method of detecting HCV genomes in formalin-fixed paraffin cardiac specimens has enabled us to widen our research into HCV infection and has been helpful in identifying the presence of HCV infection in cardiac myopathic disorders. (Lab Invest 2000, 80:1137-1142.

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confidence: 90%

Hepatitis C Virus from the Hearts of Patients with Myocarditis and Cardiomyopathy

Matsumori

Yutani

Ikeda

et al. 2000

Laboratory Investigation

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“…1,2 It has been demonstrated that the detection of EV RNA in myocardium of DCM patients is associated with adverse prognosis. 3 In particular, the presence of minus-strand EV RNA indicates active viral replication, and plays a role in the development of myocardial injury in DCM.…”

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confidence: 99%

Toll-like receptor 4 is expressed with enteroviral replication in myocardium from patients with dilated cardiomyopathy

Satoh

Nakamura

Akatsu

et al. 2004

Laboratory Investigation

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Expressions of innate immune response proteins, most notably proinflammatory cytokines, against enteroviral (EV) infection have been documented in the heart of human dilated cardiomyopathy (DCM). Toll-like receptor 4 (TLR4) activates signaling pathways leading to the expression of proinflammatory cytokines implicated the etiology of DCM. We sought to determine whether EV replication activates TLR4-dependent immune response in myocardium obtained from patients with DCM. Endomyocardial biopsy tissues were obtained from 56 patients with DCM and 10 controls. Levels of plus-and minus-strand EV RNA and TLR4 mRNA were measured by real-time RT-PCR. Immunohistochemical analysis was performed to identify the cellular source of EV capsid protein VP1 and TLR4. Both plus-and minus-strand EV RNA were detected in 19 DCM patients (34%). Neither strand of EV RNA was detected in controls. TLR4 mRNA levels were higher in DCM patients than in controls (Po0.001). A positive correlation was found between TLR4 levels and each strand type of EV RNA in EV RNApositive patients (plus-strand vs TLR4: r ¼ 0.69, Po0.001; minus-strand vs TLR4: r ¼ 0.65, P ¼ 0.002). VP1/TLR4 double staining showed extensive colocalization of VP1 and TLR4 proteins in cytoplasm of cardiac myocytes in myocardium obtained from DCM patients. EV RNA-positive patients showed lower systolic function and larger ventricular volume compared with EV RNA-negative patients left ventricular ejection fraction (LVEF): P ¼ 0.002; left ventricular end-systolic diameter (LVESD): P ¼ 0.004). The DCM subgroup with high TLR4 levels showed lower LVEF and larger LVESD than the subgroup with TLR4 levels (both Po0.001). This study suggests that myocardial expression of TLR4 associates with EV replication in human DCM. EV RNA and TLR4 mRNA levels may correlate with LV dysfunction in DCM. The expression of TLR4 against EV replication may be involved in the pathogenesis of DCM.

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“…Lack of knowledge concerning this causal factor leads to frequent diagnosis of idiopathic dilated cardiomyopathy; however, advances in viraldetection methods have made chronic virus infection an etiological possibility. Enterovirus and coxsackie-B3 and B4-virus were the most widely related to myocarditis that progressed to dilated cardiomyopathy [28]. However, a recent study, based on endocardial biopsy of individuals with left ventricular systolic dysfunction, detected a high prevalence of the cardiac parvovirus B19 viral genome, revealing a strong association between this viral agent and IDC [29].…”

Section: Discussionmentioning

confidence: 99%

Is hepatitis C virus a cause of idiopathic dilated cardiomyopathy? A systematic review of literature

Reis¹,

Sousa²,

Oliveira³

et al. 2006

Braz J Infect Dis

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Recent studies have suggested that some patients with idiopathic dilated cardiomyopathy (IDC) are also afflicted with insidious forms of viral myocarditis. Participation of hepatitis C virus (HCV) in this process has been postulated. The objective of this study was to evaluate a possible association between hepatitis C virus and idiopathic dilated cardiomyopathy. Systematic review of the literature using electronic databases (MEDLINE, EMBASES, LILACS and COCHRANE) for the period from 1995 to 2005, limited to papers published in English, Spanish and Portuguese. Sixty-two papers were found, of which six were in accordance with the proposed methodology. After selection, the articles were classified by quality of data and number of variables studied. Most of the patients were male adults from 31 and 75 years old, who had ischemic cardiopathy excluded as etiology of the dilated cardiomyopathy. A significant association between dilated cardiomyopathy and hepatitis C virus was found in only two papers, both from Japan and by the same author. Most of the papers received low classifications, as they did not fulfill the systematization criteria.

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Detection of Coxsackie-B-Virus-Specific Rna Sequences in Myocardial Biopsy Samples From Patients With Myocarditis and Dilated Cardiomyopathy

Cited by 558 publications

References 14 publications

Hepatitis C Virus from the Hearts of Patients with Myocarditis and Cardiomyopathy

Hepatitis C Virus from the Hearts of Patients with Myocarditis and Cardiomyopathy

Toll-like receptor 4 is expressed with enteroviral replication in myocardium from patients with dilated cardiomyopathy

Is hepatitis C virus a cause of idiopathic dilated cardiomyopathy? A systematic review of literature

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