Cardioviruses cause diseases in many animals including, in rare cases, humans. Although they share common features with all picornaviruses, cardioviruses have unique properties that distinguish them from other family members, including enteroviruses. One feature shared by all picornaviruses is the covalent attachment of VPg to the 5' end of genomic RNA via a phosphotyrosyl linkage. For enteroviruses, this linkage is cleaved by a host cell protein, TDP2. Since TDP2 is divergently required during enterovirus infections, we determined if TDP2 is necessary during infection by the prototype cardiovirus, EMCV. We found that EMCV yields are reduced in the absence of TDP2. We observed a decrease in viral protein accumulation and viral RNA replication in the absence of TDP2. In contrast to enterovirus infections, we found that TDP2 is modified at peak times of EMCV infection. This finding suggests a unique mechanism for cardioviruses to regulate TDP2 activity during infection.

中文翻译：

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心血管病毒感染细胞中的VPg解链酶/ TDP2：重新定位和蛋白水解裂解。

心脏病毒在许多动物中引起疾病​​，包括在极少数情况下的人类。尽管它们与所有小核糖核酸病毒具有共同的特征，但心脏病毒具有独特的属性，可将其与其他家族成员（包括肠病毒）区分开来。所有小核糖核酸病毒共有的一个特征是VPg通过磷酸酪氨酰键与基因组RNA的5'端共价结合。对于肠病毒，该连接被宿主细胞蛋白TDP2切割。由于肠道病毒感染期间需要TDP2，因此我们确定原型心脏病毒EMCV在感染期间是否需要TDP2。我们发现在没有TDP2的情况下EMCV产量会降低。我们观察到在没有TDP2的情况下病毒蛋白质积累和病毒RNA复制的减少。与肠病毒感染相反，我们发现TDP2在EMCV感染的高峰时间被修饰。该发现提示心脏病毒在感染过程中调节TDP2活性的独特机制。