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Topological implications of DNA tumor viral episomes

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초록

A persistent DNA tumor virus infection transforms normal cellsinto cancer cells by either integrating its genome into hostchromosomes or retaining it as an extrachromosomal entitycalled episome. Viruses have evolved mechanisms for attachingepisomes to infected host cell chromatin to efficiently segregatethe viral genome during mitosis. It has been reported that viralepisome can affect the gene expression of the host chromosomesthrough interactions between viral episomes and epigenetic regulatoryhost factors. This mini review summarizes our currentknowledge of the tethering sites of viral episomes, such asEBV, KSHV, and HBV, on host chromosomes analyzed bythree-dimensional genomic tools.

Abstract

A persistent DNA tumor virus infection transforms normal cellsinto cancer cells by either integrating its genome into hostchromosomes or retaining it as an extrachromosomal entitycalled episome. Viruses have evolved mechanisms for attachingepisomes to infected host cell chromatin to efficiently segregatethe viral genome during mitosis. It has been reported that viralepisome can affect the gene expression of the host chromosomesthrough interactions between viral episomes and epigenetic regulatoryhost factors. This mini review summarizes our currentknowledge of the tethering sites of viral episomes, such asEBV, KSHV, and HBV, on host chromosomes analyzed bythree-dimensional genomic tools.

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