Viruses must interact with their hosts in order to replicate; these interactions often provoke the evolutionarily conserved response to DNA damage, known as the DNA damage response (DDR). The DDR can be activated by incoming viral DNA, during the integration of retroviruses, or in response to the aberrant DNA structures generated upon replication of DNA viruses. Furthermore, DNA and RNA viral proteins can induce the DDR by promoting inappropriate S phase entry, by modifying cellular DDR factors directly, or by unintentionally targeting host DNA. The DDR may be antiviral, although viruses often require proximal DDR activation of repair and recombination factors to facilitate replication as well as downstream DDR signaling suppression to ensure cell survival. An unintended consequence of DDR attenuation during infection is the long-term survival and proliferation of precancerous cells. Therefore, the molecular basis for DDR activation and attenuation by viruses remains an important area of study that will likely provide key insights into how viruses have evolved with their hosts.

中文翻译：

---

病毒和DNA损伤反应：激活和拮抗作用。

病毒必须与其主机交互才能复制；这些相互作用经常引起对DNA损伤的进化保守反应，即DNA损伤反应（DDR）。在逆转录病毒整合过程中，或响应DNA病毒复制后产生的异常DNA结构，DDR可以被传入的病毒DNA激活。此外，DNA和RNA病毒蛋白可通过促进不适当的S期进入，直接修饰细胞DDR因子或无意靶向宿主DNA来诱导DDR。DDR可能是抗病毒的，尽管病毒通常需要近端DDR激活修复和重组因子以促进复制以及下游DDR信号抑制，以确保细胞存活。DDR在感染期间衰减的意外结果是癌前细胞的长期存活和增殖。因此，病毒激活和减弱DDR的分子基础仍然是一个重要的研究领域，可能会提供有关病毒如何随宿主进化的关键见解。