Papillomaviruses enter basal cells of stratified epithelia. Assembly of new virions occurs in infected cells during terminal differentiation. This unique biology is reflected in the mechanism of entry. Extracellularly, the interaction of nonenveloped capsids with several host cell proteins, after binding, results in discrete conformational changes. Asynchronous internalization occurs over several hours by an endocytic mechanism related to, but distinct from macropinocytosis. Intracellular trafficking leads virions through the endosomal system, and from late endosomes to the trans-Golgi-network, before nuclear delivery. Here, we discuss the existing data with the aim to synthesize an integrated model of the stepwise process of entry, thereby highlighting key open questions. Additionally, we relate data from experiments with cultured cells to in vivo results.

乳头瘤病毒进入复层上皮的基底细胞。新病毒粒子的组装发生在受感染细胞的终末分化过程中。这种独特的生物学特性体现在进入机制上。在细胞外，无包膜衣壳与几种宿主细胞蛋白的相互作用在结合后导致离散的构象变化。异步内化通过与巨胞饮作用相关但又不同的内吞机制在几个小时内发生。在核递送之前，细胞内运输引导病毒体穿过内体系统，并从晚期内体到达跨高尔基体网络。在这里，我们讨论现有数据，旨在综合逐步进入过程的集成模型，从而突出关键的开放问题。此外，我们还将培养细胞实验的数据与体内结果联系起来。