Pyeon Dohun, Pearce Shane M, Lank Simon M, Ahlquist Paul, Lambert Paul F
McArdle Laboratory for Cancer Research, University of Wisconsin-Madison, Madison, WI, USA.
PLoS Pathog. 2009 Feb;5(2):e1000318. doi: 10.1371/journal.ppat.1000318. Epub 2009 Feb 27.
Human papillomaviruses (HPVs) are DNA viruses associated with major human cancers. As such there is a strong interest in developing new means, such as vaccines and microbicides, to prevent HPV infections. Developing the latter requires a better understanding of the infectious life cycle of HPVs. The HPV infectious life cycle is closely linked to the differentiation state of the stratified epithelium it infects, with progeny virus only made in the terminally differentiating suprabasal compartment. It has long been recognized that HPV must first establish its infection within the basal layer of stratified epithelium, but why this is the case has not been understood. In part this restriction might reflect specificity of expression of entry receptors. However, this hypothesis could not fully explain the differentiation restriction of HPV infection, since many cell types can be infected with HPVs in monolayer cell culture. Here, we used chemical biology approaches to reveal that cell cycle progression through mitosis is critical for HPV infection. Using infectious HPV16 particles containing the intact viral genome, G1-synchronized human keratinocytes as hosts, and early viral gene expression as a readout for infection, we learned that the recipient cell must enter M phase (mitosis) for HPV infection to take place. Late M phase inhibitors had no effect on infection, whereas G1, S, G2, and early M phase cell cycle inhibitors efficiently prevented infection. We conclude that host cells need to pass through early prophase for successful onset of transcription of the HPV encapsidated genes. These findings provide one reason why HPVs initially establish infections in the basal compartment of stratified epithelia. Only this compartment of the epithelium contains cells progressing through the cell cycle, and therefore it is only in these cells that HPVs can establish their infection. By defining a major condition for cell susceptibility to HPV infection, these results also have potentially important implications for HPV control.
人乳头瘤病毒(HPVs)是与人类主要癌症相关的DNA病毒。因此,人们对开发新的预防手段,如疫苗和杀菌剂,以预防HPV感染有着浓厚的兴趣。开发后者需要更好地了解HPVs的感染生命周期。HPV的感染生命周期与它所感染的复层上皮的分化状态密切相关,子代病毒仅在终末分化的基底上层隔室中产生。长期以来,人们一直认识到HPV必须首先在复层上皮的基底层建立感染,但其中的原因尚不清楚。部分原因可能反映了进入受体表达的特异性。然而,这一假设无法完全解释HPV感染的分化限制,因为在单层细胞培养中,许多细胞类型都能被HPVs感染。在此,我们使用化学生物学方法揭示,通过有丝分裂的细胞周期进程对HPV感染至关重要。我们以含有完整病毒基因组的感染性HPV16颗粒、G1期同步化的人角质形成细胞作为宿主,并以早期病毒基因表达作为感染的读数,发现受体细胞必须进入M期(有丝分裂)才能发生HPV感染。M期末期抑制剂对感染没有影响,而G1期、S期、G2期和M期早期细胞周期抑制剂能有效预防感染。我们得出结论,宿主细胞需要通过前期早期才能成功启动HPV衣壳化基因的转录。这些发现提供了一个理由,解释了为什么HPVs最初在复层上皮的基底层建立感染。只有上皮的这个隔室包含经历细胞周期进程的细胞,因此只有在这些细胞中HPVs才能建立感染。通过确定细胞对HPV感染易感性的一个主要条件,这些结果对HPV的控制也可能具有重要意义。