Virus–host cell interactions include several skirmishes between the virus and its host, and the DNA damage response (DDR) network is one of their important battlegrounds. Although some aspects of the DDR are exploited by adenovirus (Ad) to improve virus replication, especially at the early phase of infection, a large body of evidence demonstrates that Ad devotes many of its proteins, including E1B-55K, E4orf3, E4orf4, E4orf6, and core protein VII, and utilizes varied mechanisms to inhibit the DDR. These findings indicate that the DDR would strongly restrict Ad replication if allowed to function efficiently. Various Ad serotypes inactivate DNA damage sensors, including the Mre11-Rad50-Nbs1 (MRN) complex, DNA-dependent protein kinase (DNA-PK), and Poly (ADP-ribose) polymerase 1 (PARP-1). As a result, these viruses inhibit signaling via DDR transducers, such as the ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR) kinases, to downstream effectors. The different Ad serotypes utilize both shared and distinct mechanisms to inhibit various branches of the DDR. The aim of this review is to understand the interactions between Ad proteins and the DDR and to appreciate how these interactions contribute to viral replication.

中文翻译：

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守卫！腺病毒与DNA损伤反应之间的相互作用。

病毒与宿主细胞的相互作用包括病毒与其宿主之间的几次小冲突，DNA损伤反应（DDR）网络是其重要战场之一。尽管DDR的某些方面已被腺病毒（Ad）所利用，以改善病毒复制，尤其是在感染的早期，但大量证据表明Ad致力于其许多蛋白质，包括E1B-55K，E4orf3，E4orf4，E4orf6和核心蛋白VII，并利用多种机制抑制DDR。这些发现表明，如果允许DDR有效运行，DDR将强烈限制Ad复制。多种Ad血清型可灭活DNA损伤传感器，包括Mre11-Rad50-Nbs1（MRN）复合物，DNA依赖性蛋白激酶（DNA-PK）和聚（ADP-核糖）聚合酶1（PARP-1）。结果是，这些病毒通过DDR传感器（例如共济失调-毛细血管扩张突变（ATM）以及与ATM和Rad3相关（ATR）的激酶）抑制信号传导至下游效应子。不同的Ad血清型利用共享机制和独特机制来抑制DDR的各个分支。本文的目的是了解Ad蛋白与DDR之间的相互作用，并了解这些相互作用如何促进病毒复制。