PDF(Pubmed)
Abstract：
Persistent infection with high-risk human papillomaviruses (HR-HPVs) is the causal factor in over 99 % of cervical cancer cases, and a significant proportion of oropharyngeal and anogenital cancers. The key drivers of HPV-mediated transformation are the oncoproteins E5, E6 and E7. Together, they act to prolong cell-cycle progression, delay differentiation and inhibit apoptosis in the host keratinocyte cell in order to generate an environment permissive for viral replication. The oncoproteins also have key roles in mediating evasion of the host immune response, enabling infection to persist. Moreover, prolonged infection within the cellular environment established by the HR-HPV oncoproteins can lead to the acquisition of host genetic mutations, eventually culminating in transformation to malignancy. In this review, we outline the many ways in which the HR-HPV oncoproteins manipulate the host cellular environment, focusing on how these activities can contribute to carcinogenesis.
摘要：
高危型人乳头瘤病毒(HR-HPVs)持续感染是99%以上宫颈癌病例的致病因素。和相当比例的口咽和肛门生殖器癌症。HPV介导的转化的关键驱动因素是癌蛋白E5、E6和E7。一起,它们的作用是延长细胞周期进程，延迟分化并抑制宿主角质形成细胞的凋亡，以产生允许病毒复制的环境。癌蛋白在介导宿主免疫应答的逃避中也具有关键作用。使感染持续。此外，由HR-HPV癌蛋白建立的细胞环境内的长期感染可导致获得宿主基因突变，最终转化为恶性肿瘤。在这次审查中,我们概述了HR-HPV癌蛋白操纵宿主细胞环境的许多方式，专注于这些活动如何促进致癌作用。
