Type B coxsackieviruses (CVB) can cause myocarditis and dilated cardiomyopathy (DCM), a potentially-fatal sequela that has been correlated to the persistence of viral RNA. Herein, we demonstrate that cardiac RNA persistence can be established even after an inapparent primary infection. Using an inducible Cre/lox mouse model, we ask: (i) Does persistent CVB3 RNA cause ongoing immune activation? (ii) If T1IFN signaling into cardiomyocytes is ablated after RNA persistence is established, is there any change in the abundance of persistent CVB3 RNA and/or does cytopathic infectious virus re-emerge? (iii) Does this loss of T1IFN responsiveness by cardiomyocytes lead to the recurrence/exacerbation of myocarditis? Our findings suggest that persistent enteroviral RNAs probably do not contribute to ongoing myocardial disease, and are more likely to be the fading remnants of a recent, possibly sub-clinical, primary infection which may have set in motion the process that ultimately ends in DCM.

B型柯萨奇病毒（CVB）会引起心肌炎和扩张型心肌病（DCM），这是一种致命的后遗症，与病毒RNA的持久性有关。在此，我们证明即使在不明显的原发感染后也可以建立心脏RNA持久性。使用可诱导的Cre / lox小鼠模型，我们问：（i）持久性CVB3 RNA是否会引起持续的免疫激活？（ii）如果在建立RNA持久性后消除了向心肌细胞的T1IFN信号转导，持久性CVB3 RNA的丰度是否有任何变化和/或细胞病变的传染性病毒是否会重新出现？（iii）心肌细胞对T1IFN反应性的丧失会导致心肌炎的复发/加重吗？我们的研究结果表明，持续存在的肠病毒RNA可能不会导致正在进行的心肌疾病，