There are extensive interactions between viruses and the host DNA damage response (DDR) machinery. The outcome of these interactions includes not only direct effects on viral nucleic acids and genome replication, but also the activation of host stress response signalling pathways that can have further, indirect effects on viral life cycles. The non-homologous end-joining (NHEJ) pathway is responsible for the rapid and imprecise repair of DNA double-stranded breaks in the nucleus that would otherwise be highly toxic. Whilst directly repairing DNA, components of the NHEJ machinery, in particular the DNA-dependent protein kinase (DNA-PK), can activate a raft of downstream signalling events that activate antiviral, cell cycle checkpoint and apoptosis pathways. This combination of possible outcomes results in NHEJ being pro- or antiviral depending on the infection. In this review we will describe the broad range of interactions between NHEJ components and viruses and their consequences for both host and pathogen.

中文翻译：

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具有非同源末端连接的病毒相互作用：一场捉迷藏的游戏。


病毒和宿主 DNA 损伤反应 (DDR) 机制之间存在广泛的相互作用。这些相互作用的结果不仅包括对病毒核酸和基因组复制的直接影响，还包括宿主应激反应信号通路的激活，这可能对病毒生命周期产生进一步的间接影响。非同源末端连接 (NHEJ) 途径负责快速且不精确地修复细胞核中的 DNA 双链断裂，否则这些断裂将具有剧毒。在直接修复 DNA 的同时，NHEJ 机制的组件，特别是 DNA 依赖性蛋白激酶 (DNA-PK)，可以激活一系列下游信号转导事件，从而激活抗病毒、细胞周期检查点和细胞凋亡途径。这种可能结果的组合导致 NHEJ 根据感染情况而具有促病毒或抗病毒作用。在这篇综述中，我们将描述 NHEJ 成分和病毒之间广泛的相互作用及其对宿主和病原体的影响。