Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
J Virol. 2019 Jan 4;93(2). doi: 10.1128/JVI.01012-17. Print 2019 Jan 15.
The inactivation of critical cell cycle checkpoints by the human papillomavirus (HPV) oncoprotein E7 results in replication stress (RS) that leads to genomic instability in premalignant lesions. Intriguingly, RS tolerance is achieved through several mechanisms, enabling HPV to exploit the cellular RS response for viral replication and to facilitate viral persistence in the presence of DNA damage. As such, inhibitors of the RS response pathway may provide a novel approach to target HPV-associated lesions and cancers.
人乳头瘤病毒（HPV）致癌蛋白 E7 使关键细胞周期检验点失活，导致复制应激（RS），从而导致癌前病变中的基因组不稳定。有趣的是，通过几种机制实现了 RS 耐受，使 HPV 能够利用细胞 RS 反应进行病毒复制，并在存在 DNA 损伤的情况下促进病毒持续存在。因此，RS 反应途径的抑制剂可能为靶向 HPV 相关病变和癌症提供一种新方法。
