Advances in the Understanding of Myocarditis

Liu, Peter P.; Mason, Jay W.

doi:10.1161/hc3401.095198

Cited by 442 publications

(288 citation statements)

References 73 publications

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“…Infections of susceptible mouse strains or immuno-compromised animals with CVB3 faithfully recapitulate many aspects of myocarditis and DCM in humans. [9][10][11] In mice, myocarditis is a multi-stage process beginning with viremia, immediately followed by infiltration of the heart by innate effectors. In this early acute phase, a combination of direct viral cytopathy, intense cytokine production 12 and inflammatory infiltration of the myocardium by innate effectors including macrophages and natural killer cells, contribute to the early myocardial damage.…”

Section: Introductionmentioning

confidence: 99%

Complex genetic control of host susceptibility to coxsackievirus B3-induced myocarditis

et al. 2007

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The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. We have used a model of infection with coxsackievirus B3 (CVB3) to characterize the contribution of host genetics to viral myocarditis in mice of different genetic backgrounds but with a common H2 haplotype: A/J and B10.A-H2 a .Here we have used Evans blue dye as a quantitative biomarker for susceptibility to CVB3-induced myocarditis in addition to histopathological semiquantitative measures. We have found evidence of linkage between susceptibility to viral myocarditis and three loci. A locus on chromosome 1 centered on D1Mit200 was linked to sarcolemmal disruption in males (P ¼ 0.00005), a second locus on chromosome 4 centered on D4Mit81 was also linked to sarcolemmal disruption in males (P ¼ 0.0022). A third locus on distal chromosome 3 centered on D3Mit19 was linked to myocardial infiltration, with a logarithm of odds (LOD) score of 4.7 (P ¼ 0.0045), as well as sarcolemmal disruption in females (P ¼ 0.0015). These results provide strong evidence for the presence of loci contributing to the susceptibility of mice to viral myocarditis.

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Section: Introductionmentioning

confidence: 99%

Complex genetic control of host susceptibility to coxsackievirus B3-induced myocarditis

et al. 2007

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“…1 The pathogenesis of CVB3-induced myocarditis is triphasic: (1) virus infection that directly damages myocytes, (2) an immune phase with accompanying inflammatory cell infiltration, and (3) repair, fibrosis, and cardiac remodeling. 2 Evidence supporting CVB as an important causative agent in myocarditis includes in situ and polymerase chain reaction (PCR) detection of viral RNA in hearts of patients with myocarditis, [3][4][5] isolation of infectious virus from acute myocarditic patients, 6 and demonstration of virus-induced cell death in CVB3-infected myocytes. 7 The type I IFNs (␣, ␤, , and ) are cytokines that interact with and signal through a common receptor complex composed of 2 transmembrane chains, IFNAR1 and IFNAR2.…”

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confidence: 99%

Protective Role for Interferon-β in Coxsackievirus B3 Infection

et al. 2004

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Background-Coxsackievirus-induced myocarditis can be a serious cause of heart failure. In the absence of a specific antiviral therapy, modulating the host immune response may be protective. Interferons (IFNs)-␣ and -␤ perform a fundamental role in innate and adaptive antiviral responses, thereby presenting as candidate therapeutics for coxsackievirus infections. Methods and Results-To examine the contribution of IFN-␤ in protection from coxsackievirus B3 (CVB3) infection, mice lacking the IFN-␤ gene were infected with 10 3 plaque-forming units of CVB3. In contrast to wild-type mice that exhibit an intact IFN-␤ response, we observed increased susceptibility to infection (70% mortality), a downregulation of IFN-stimulated gene targets (2Ј-5Ј oligoadenylate synthetase, serine/threonine protein kinase, the GTPase Mx), and cardiomyocyte breakdown and disruption in the IFN-␤ Ϫ/Ϫ mice. Conclusions-Viewed

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“…Дальнейшее развитие и прогрессирование миокардиального повреждения зависит от выражен-ности и направленности иммунных и особенно ауто-иммунных реакций. Установлено, что у части больных (по различным данным от 40 до 50 %) ДКМП развива-ется после вирусного миокардита [13]. В литературе аспект ЭД у пациентов с ДКМП изучен более подробно.…”

Section: Discussionunclassified

“…При ДКМП ведущая роль будет отводиться вирусным агентам с последующим каскадом аутоиммуных реакций, особенно на ранних этапах формирования, что в последующем приведет к ЭД [13]. У пациентов с ФЕЖС ведущую роль может играть наличие кондуита и много-этапная хирургическая коррекция, которые, в свою оче-редь, являются постоянным триггерным фактором ауто-иммунного процесса.…”

Section: оригинальные статьи §unclassified