Division of Infectious Diseases, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, MA 02115, USA.
Curr Opin Virol. 2012 Aug;2(4):459-66. doi: 10.1016/j.coviro.2012.05.004. Epub 2012 Jun 2.
A small group of human papillomaviruses (HPVs) cause almost all cervical carcinoma and a significant percentage of other anogenital tract and oral carcinoma. Another group of HPVs causes non-melanoma skin cancers in genetically predisposed or immune suppressed patients upon UV exposure. HPV genome replication requires the host cell's DNA synthesis machinery and HPVs encode proteins that maintain differentiated epithelial cells in a replication competent state. The resulting rewiring of cellular signal transduction circuits triggers several innate cellular tumor suppressor responses that HPVs need to inactivate in order to establish persistent and/or productive infections. This review emphasizes this interplay between virus and the infected host cells and points out biological similarities and differences between different groups of HPVs.
一小部分人乳头瘤病毒（HPV）几乎会引起所有宫颈癌，以及相当大比例的其他生殖器官和口腔癌。另一组 HPV 会导致具有遗传易感性或免疫抑制的患者在暴露于 UV 后患上非黑色素瘤皮肤癌。HPV 基因组复制需要宿主细胞的 DNA 合成机制，HPV 编码的蛋白可使分化的上皮细胞维持在具有复制能力的状态。由此引发的细胞信号转导通路的重新布线触发了几种先天的细胞肿瘤抑制反应，HPV 需要使其失活，以建立持续性和/或生产性感染。这篇综述强调了病毒与受感染宿主细胞之间的这种相互作用，并指出了不同 HPV 组之间的生物学相似性和差异性。
