Chapman N M, Kim K S
University of Nebraska Medical Center, Omaha, NE 68198-6495, USA
Curr Top Microbiol Immunol. 2008;323:275-92. doi: 10.1007/978-3-540-75546-3_13.
Enteroviral infection of the heart has been noted in a significant proportion of cases of myocarditis and dilated cardiomyopathy. The presence of enterovirus RNA at stages of disease after acute infection and correlation of enterovirus replication with worse clinical outcome suggests continued replication of the virus is involved in the progression of the disease. This finding is mirrored by the murine model of coxsackievirus B3 myocarditis, in which virus persists through the evolution of the virus to a terminally deleted defective form which persists in the myocardium. Studies of the mechanism of induction of myocarditis by coxsackievirus B3 require assessment of the effects of alterations of the immune response upon virus persistence in this form. As expression of viral proteins in the heart have been shown to generate significant impairment of cardiomyocyte function and promote generation of dilated cardiomyopathy, the role of virus persistence is likely to include direct effects of viral replication as well as induction of inflammation in the heart. Factors that control the extent of cardiac infection with terminally deleted enteroviruses and the relative roles of continued immune response of the virus vs viral modification of cardiac function need to be measured to find effective therapies for the human disease.
在相当比例的心肌炎和扩张型心肌病病例中已发现心脏的肠道病毒感染。在急性感染后的疾病阶段存在肠道病毒RNA，以及肠道病毒复制与更差临床结果的相关性表明，病毒的持续复制参与了疾病的进展。柯萨奇病毒B3心肌炎的小鼠模型也反映了这一发现，在该模型中，病毒通过演变成末端缺失的缺陷形式而持续存在于心肌中。对柯萨奇病毒B3诱导心肌炎机制的研究需要评估免疫反应改变对这种形式的病毒持续存在的影响。由于已表明心脏中病毒蛋白的表达会严重损害心肌细胞功能并促进扩张型心肌病的发生，病毒持续存在的作用可能包括病毒复制的直接影响以及心脏炎症的诱导。需要测量控制心脏被末端缺失肠道病毒感染程度的因素，以及病毒持续免疫反应与病毒对心脏功能改变的相对作用，以找到针对人类疾病的有效疗法。
