Kalland Karl-Henning, Ke Xi-Song, Øyan Anne Margrete
The Gade Institute, University of Bergen, Norway.
APMIS. 2009 May;117(5-6):382-99. doi: 10.1111/j.1600-0463.2009.02452.x.
Viruses enter host cells in order to complete their life cycles and have evolved to exploit host cell structures, regulatory factors and mechanisms. The virus and host cell interactions have consequences at multiple levels, spanning from evolution through disease to models and tools for scientific discovery and treatment. Virus-induced human cancers arise after a long duration of time and are monoclonal or oligoclonal in origin. Cancer is therefore a side effect rather than an essential part of viral infections in humans. Still, 15-20% of all human cancers are caused by viruses. A review of tumour virology shows its close integration in cancer research. Viral tools and experimental models have been indispensible for the progress of molecular biology. In particular, retroviruses and DNA tumour viruses have played major roles in our present understanding of the molecular biology of both viruses and the host. Recently, additional complex relationships due to virus and host co-evolution have appeared and may lead to a further understanding of the overall regulation of gene expression programmes in cancer.
病毒进入宿主细胞以完成其生命周期,并已进化到利用宿主细胞结构、调节因子和机制。病毒与宿主细胞的相互作用在多个层面产生影响,从进化到疾病,再到科学发现和治疗的模型与工具。病毒诱发的人类癌症经过很长时间才出现,起源上是单克隆或寡克隆的。因此,癌症是病毒感染人类的副作用而非必要组成部分。尽管如此,所有人类癌症中仍有15% - 20%是由病毒引起的。肿瘤病毒学综述表明其在癌症研究中紧密结合。病毒工具和实验模型对分子生物学的进展不可或缺。特别是逆转录病毒和DNA肿瘤病毒在我们目前对病毒和宿主分子生物学的理解中发挥了主要作用。最近,由于病毒与宿主共同进化而出现的其他复杂关系可能会进一步加深我们对癌症中基因表达程序整体调控的理解。