G. Fung, Honglin Luo, Ye Qiu, Decheng Yang, Bruce McManus
{"title":"Myocarditis","authors":"G. Fung, Honglin Luo, Ye Qiu, Decheng Yang, Bruce McManus","doi":"10.1002/9781119547808.ch27","DOIUrl":null,"url":null,"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","PeriodicalId":341699,"journal":{"name":"Rapid Cardiac Care","volume":"46 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2018-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Rapid Cardiac Care","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/9781119547808.ch27","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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