Feeney Katherine M, Parish Joanna L
Bute Medical School, University of St Andrews, St Andrews, Fife KY16 9TS, UK.
Proc Biol Sci. 2009 May 7;276(1662):1535-44. doi: 10.1098/rspb.2008.1642. Epub 2009 Jan 20.
Viruses that maintain their genomes as extrachromosomal circular DNA molecules and establish infection in actively dividing cells must ensure retention of their genomes within the nuclear envelope in order to prevent genome loss. The loss of nuclear membrane integrity during mitosis dictates that paired host cell chromosomes are captured and organized by the mitotic spindle apparatus before segregation to daughter cells. This prevents inaccurate chromosomal segregation and loss of genetic material. A similar mechanism may also exist for the nuclear retention of extrachromosomal viral genomes or episomes during mitosis, particularly for genomes maintained at a low copy number in latent infections. It has been heavily debated whether such a mechanism exists and to what extent this mechanism is conserved among diverse viruses. Research over the last two decades has provided a wealth of information regarding the mechanisms by which specific tumour viruses evade mitotic and DNA damage checkpoints. Here, we discuss the similarities and differences in how specific viruses tether episomal genomes to host cell chromosomes during mitosis to ensure long-term persistence.
那些将其基因组维持为染色体外环状DNA分子并在活跃分裂的细胞中建立感染的病毒，必须确保其基因组保留在核膜内，以防止基因组丢失。有丝分裂期间核膜完整性的丧失表明，配对的宿主细胞染色体在分离到子细胞之前，会被有丝分裂纺锤体装置捕获并组织起来。这可防止染色体分离不准确和遗传物质丢失。在有丝分裂期间，染色体外病毒基因组或附加体的核保留可能也存在类似机制，特别是对于在潜伏感染中以低拷贝数维持的基因组。是否存在这样一种机制以及该机制在不同病毒中的保守程度如何，一直存在激烈争论。过去二十年的研究提供了大量关于特定肿瘤病毒逃避有丝分裂和DNA损伤检查点机制的信息。在这里，我们讨论了特定病毒在有丝分裂期间如何将附加体基因组与宿主细胞染色体相连以确保长期持续存在的异同。
