The human DNA damage response (DDR) is a complex signaling network constituting many factors responsible for the preservation of genomic integrity. Human polyomaviruses (HPyVs) are able to harness the DDR machinery during their infectious cycle by expressing an array of tumor (T) antigens. These molecular interactions between human polyomavirus T antigens and the DDR create conditions that promote viral replication at the expense of host genomic stability to cause disease as well as carcinogenesis in the cases of the Merkel cell polyomavirus and BK polyomavirus. This review focuses on the six HPyVs with disease association, emphasizing strain-dependent differences in their selective manipulation of the DDR. Appreciation of the HPyV-DDR interface at a molecular scale is conducive to the development of novel therapeutic approaches.

中文翻译：

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人类多瘤病毒对宿主DNA损伤反应的调节。

人类DNA损伤反应（DDR）是一个复杂的信号网络，由许多因素构成，负责保存基因组完整性。人类多瘤病毒（HPyV）能够通过表达一系列肿瘤（T）抗原来利用DDR机制进行感染。人类多瘤病毒T抗原和DDR之间的这些分子相互作用创造了促进病毒复制的条件，但在默克尔细胞多瘤病毒和BK多瘤病毒的情况下，以宿主基因组稳定性为代价导致疾病以及致癌作用。这篇综述着重于与疾病相关的六个HPyVs，强调了它们对DDR的选择性操纵中依赖菌株的差异。在分子水平上对HPyV-DDR接口的欣赏有助于开发新的治疗方法。