Spriggs Chelsey C, Laimins Laimonis A
Department of Microbiology-Immunology, Northwestern University, Feinberg School of Medicine, 303 E. Chicago Ave., Chicago, IL 60611, USA.
Viruses. 2017 Aug 18;9(8):232. doi: 10.3390/v9080232.
High-risk human papillomaviruses (HPVs) are the causative agents of cervical and other genital cancers. In addition, HPV infections are associated with the development of many oropharyngeal cancers. HPVs activate and repress a number of host cellular pathways to promote their viral life cycles, including those of the DNA damage response. High-risk HPVs activate the ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related (ATR) DNA damage repair pathways, which are essential for viral replication (particularly differentiation-dependent genome amplification). These DNA repair pathways are critical in maintaining host genomic integrity and stability and are often dysregulated or mutated in human cancers. Understanding how these pathways contribute to HPV replication and transformation may lead to the identification of new therapeutic targets for the treatment of existing HPV infections.
高危型人乳头瘤病毒（HPV）是宫颈癌和其他生殖器癌症的致病因子。此外，HPV感染与许多口咽癌的发生有关。HPV激活并抑制多种宿主细胞途径以促进其病毒生命周期，包括DNA损伤反应途径。高危型HPV激活共济失调毛细血管扩张症突变（ATM）和ATM及Rad3相关（ATR）DNA损伤修复途径，这些途径对病毒复制（特别是依赖分化的基因组扩增）至关重要。这些DNA修复途径对于维持宿主基因组的完整性和稳定性至关重要，并且在人类癌症中常常失调或发生突变。了解这些途径如何促进HPV复制和转化可能会导致识别出治疗现有HPV感染的新治疗靶点。
