整合分析揭示 HPV11、-16 和 -45 早期感染的新策略。
Integrative analyses reveal novel strategies in HPV11,-16 and -45 early infection.
机构信息
The Bioinformatics Centre, Department of Biology and Biomedical Research and Innovation Centre, Copenhagen University, Ole Maaloes Vej 5, 2200Copenhagen, Denmark.
出版信息
Sci Rep. 2012;2:515. doi: 10.1038/srep00515. Epub 2012 Jul 17.
The interaction between human papillomavirus (HPV) and host cells is not well understood. We investigate the early stage of HPV infections by global expression profiling in a cell model, in which HaCaT cells were transfected with HPV11, HPV16 or HPV45 genomes. We report the differential expression of genes not previously implicated in HPV biology, such as the PSG family and ANKRD1, and of genes implicated in the biology of other viruses, e.g. MX1, IFI44 and DDX60. Carcinogenesis-related genes, e.g. ABL2, MGLL and CYR61, were upregulated by high-risk HPV16 and -45. The integrative analysis revealed the suppression of DNA repair by HPV11 and -16, and downregulation of cytoskeleton genes by all HPV types. Various signalling pathways were affected by the HPVs: IL-2 by HPV11; JAK-STAT by HPV16; and TGF-β, NOTCH and tyrosine kinase signalling by HPV45. This study uncovered novel strategies employed by HPV to establish infection and promote uncontrolled growth.
人类乳头瘤病毒（HPV）与宿主细胞的相互作用尚未得到很好的理解。我们通过细胞模型中的全局表达谱研究 HPV 感染的早期阶段，在该模型中，HaCaT 细胞被 HPV11、HPV16 或 HPV45 基因组转染。我们报告了先前未涉及 HPV 生物学的基因的差异表达，例如 PSG 家族和 ANKRD1，以及涉及其他病毒生物学的基因的差异表达，例如 MX1、IFI44 和 DDX60。致癌相关基因，例如 ABL2、MGLL 和 CYR61，被高危 HPV16 和 -45 上调。综合分析显示 HPV11 和 -16 抑制了 DNA 修复，而所有 HPV 类型都下调了细胞骨架基因。各种信号通路受到 HPV 的影响：HPV11 影响 IL-2；HPV16 影响 JAK-STAT；HPV45 影响 TGF-β、NOTCH 和酪氨酸激酶信号通路。这项研究揭示了 HPV 用于建立感染和促进不受控制的生长的新策略。
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