Myocarditis

G. Fung, Honglin Luo, Ye Qiu, Decheng Yang, Bruce McManus
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Abstract

: Viral myocarditis remains a prominent infectious-inflammatory disease for patients throughout the lifespan. The condition presents several challenges including varied modes of clinical presentation, a range of timepoints when patients come to attention, a diversity of approaches to diagnosis, a spectrum of clinical courses, and unsettled perspectives on therapeutics in different patient settings and in the face of different viral pathogens. In this review, we examine current knowledge about viral heart disease and especially provide information on evolving understanding of mechanisms of disease and efforts by investigators to identify and evaluate potential therapeutic avenues for intervention. ( Circ Res . 2016;118:496-514. DOI: chain reaction techniques for cellular infiltrates viral presence. myocardium is provided by the findings that elimination of the coxsackievirus-adenovirus receptor (CAR) specifically in the adult mouse hearts completely blocks viral infection of myocardial cells and virus-induced inflammation in the myocardium. These CVB3-infected mice exhibit improved cardiac function, whereas other tissues (eg, pancreas and spleen) that also express CAR are CVB3 positive. This study suggests that viral infection of cardiomyocytes and consequent productive viral replication within the myocardium is required for the development of myocarditis. CAR, a transmembrane protein in the family of adhesion molecules, localized predominantly at the intercalated disc and the cell–cell junctions of the AV node in the adult heart is required for virus entry into different cell types. 79,80 Studies from independent research groups revealed an important role of the in embryonic development and the maintenance of nor-mal AV conduction and cardiac function. 79–81 The the heart of patients adult young myocarditis. In CVB3 also determined by decay-accelerating factor (CD55) coreceptor in certain cell types. 83 For CVB3 with decay-accelerating factor on the apical surface of epithelial cells the interaction between virus and CAR, which is localized to the tight junction; normally inacces-sible to virus. The underlying direct been extensively studied. molecular protein signaling
心肌炎
病毒性心肌炎仍然是患者一生中重要的感染性炎症性疾病。这种情况提出了一些挑战,包括不同的临床表现模式,患者注意到的时间点范围,诊断方法的多样性,临床过程的谱,以及不同患者环境和面对不同病毒病原体的治疗方法的不稳定观点。在这篇综述中,我们研究了目前关于病毒性心脏病的知识,特别是提供了关于疾病机制的不断发展的理解和研究人员努力识别和评估潜在的治疗干预途径的信息。(Circ Res)2016; 118:496 - 514。细胞浸润病毒存在的链式反应技术。研究发现,在成年小鼠心脏中特异性消除柯萨奇病毒-腺病毒受体(CAR)完全阻断心肌细胞的病毒感染和病毒诱导的心肌炎症。这些CVB3感染的小鼠表现出改善的心脏功能,而其他组织(如胰腺和脾脏)也表达CAR是CVB3阳性。这项研究表明,心肌细胞的病毒感染和随后在心肌内产生的病毒复制是心肌炎发展所必需的。CAR是粘附分子家族中的一种跨膜蛋白,主要定位于成人心脏内嵌盘和房室结的细胞-细胞连接处,是病毒进入不同细胞类型所必需的。来自独立研究小组的研究揭示了胚胎发育和维持正常房室传导和心脏功能的重要作用。79-81成人青年心肌炎患者的心脏。在某些细胞类型中,CVB3也由衰变加速因子(CD55)辅助受体决定。83对于在上皮细胞顶表面有加速因子的CVB3,病毒与CAR的相互作用局限于紧密连接处;病毒通常无法访问。潜在的直接因素得到了广泛的研究。分子蛋白信号
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