Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Viruses. 2022 Aug 17;14(8):1797. doi: 10.3390/v14081797.
High-risk human papillomaviruses (HR HPVs) are associated with multiple human cancers and comprise 5% of the human cancer burden. Although most infections are transient, persistent infections are a major risk factor for cancer development. The life cycle of HPV is intimately linked to epithelial differentiation. HPVs establish infection at a low copy number in the proliferating basal keratinocytes of the stratified epithelium. In contrast, the productive phase of the viral life cycle is activated upon epithelial differentiation, resulting in viral genome amplification, high levels of late gene expression, and the assembly of virions that are shed from the epithelial surface. Avoiding activation of an innate immune response during the course of infection plays a key role in promoting viral persistence as well as completion of the viral life cycle in differentiating epithelial cells. This review highlights the recent advances in our understanding of how HPVs manipulate the host cell environment, often in a type-specific manner, to suppress activation of an innate immune response to establish conditions supportive of viral replication.
高危型人乳头瘤病毒（HR HPV）与多种人类癌症相关，占人类癌症负担的 5%。虽然大多数感染是短暂的，但持续性感染是癌症发展的主要危险因素。HPV 的生命周期与上皮细胞分化密切相关。HPV 在分层上皮的增殖基底角质形成细胞中以低拷贝数建立感染。相比之下，病毒生命周期的有性阶段在上皮分化时被激活，导致病毒基因组扩增、晚期基因表达水平升高，以及从上皮表面脱落的病毒粒子的组装。在感染过程中避免激活先天免疫反应在促进病毒持续存在以及在分化的上皮细胞中完成病毒生命周期方面起着关键作用。这篇综述强调了我们对 HPV 如何操纵宿主细胞环境的理解的最新进展，通常以特定于类型的方式，以抑制先天免疫反应的激活，从而建立支持病毒复制的条件。
