Structural and Computational Biology Unit, European Molecular Biology Laboratory, 69117 Heidelberg, Germany.
Trends Biochem Sci. 2011 Mar;36(3):159-69. doi: 10.1016/j.tibs.2010.10.002. Epub 2010 Dec 9.
Viruses, as obligate intracellular parasites, are the pathogens that have the most intimate relationship with their host, and as such, their genomes have been shaped directly by interactions with the host proteome. Every step of the viral life cycle, from entry to budding, is orchestrated through interactions with cellular proteins. Accordingly, viruses will hijack and manipulate these proteins utilising any achievable mechanism. Yet, the extensive interactions of viral proteomes has yielded a conundrum: how do viruses commandeer so many diverse pathways and processes, given the obvious spatial constraints imposed by their compact genomes? One important approach is slowly being revealed, the extensive mimicry of host protein short linear motifs (SLiMs).
病毒是专性细胞内寄生的病原体,与宿主的关系最为密切,因此,它们的基因组直接受到与宿主蛋白质组相互作用的影响。从进入到出芽,病毒生命周期的每一个步骤都是通过与细胞蛋白相互作用来协调的。因此,病毒会利用任何可行的机制劫持和操纵这些蛋白。然而,病毒蛋白质组的广泛相互作用产生了一个难题:考虑到它们紧凑基因组所施加的明显空间限制,病毒是如何劫持如此多不同的途径和过程的?一种重要的方法正在慢慢被揭示,即广泛模拟宿主蛋白短线性基序(SLiMs)。