Regulation of the Innate Immune Response during the Human Papillomavirus Life Cycle.
Regulation of the Innate Immune Response during the Human Papillomavirus Life Cycle.
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DOI：
10.3390/v14081797
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发表时间：
2022-08-17
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高危人乳头瘤病毒（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，但持续感染是癌症发展的主要风险因素。HPV的生命周期与上皮分化密切相关。HPV以低拷贝数在复层上皮的增殖基底角质形成细胞中建立感染。相反，病毒生命周期的生产阶段在上皮分化时被激活，导致病毒基因组扩增、高水平的晚期基因表达和从上皮表面脱落的病毒体的组装。在感染过程中避免先天免疫应答的激活在促进病毒持续存在以及在分化上皮细胞中完成病毒生命周期中起关键作用。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，通常以类型特异性的方式，抑制先天免疫反应的激活，以建立支持病毒复制的条件。
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.