Department of Laboratory Medicine, Lund University, 221 84 Lund, Sweden.
Int J Mol Sci. 2018 Jun 12;19(6):1735. doi: 10.3390/ijms19061735.
Human papillomaviruses (HPVs) have evolved to use the DNA repair machinery to replicate its DNA genome in differentiated cells. HPV activates the DNA damage response (DDR) in infected cells. Cellular DDR factors are recruited to the HPV DNA genome and position the cellular DNA polymerase on the HPV DNA and progeny genomes are synthesized. Following HPV DNA replication, HPV late gene expression is activated. Recent research has shown that the DDR factors also interact with RNA binding proteins and affects RNA processing. DDR factors activated by DNA damage and that associate with HPV DNA can recruit splicing factors and RNA binding proteins to the HPV DNA and induce HPV late gene expression. This induction is the result of altered alternative polyadenylation and splicing of HPV messenger RNA (mRNA). HPV uses the DDR machinery to replicate its DNA genome and to activate HPV late gene expression at the level of RNA processing.
人乳头瘤病毒（HPV）已经进化到可以利用 DNA 修复机制在分化细胞中复制其 DNA 基因组。HPV 在受感染的细胞中激活 DNA 损伤反应（DDR）。细胞 DDR 因子被招募到 HPV DNA 上，并将细胞 DNA 聚合酶定位在 HPV DNA 上，然后合成前体基因组。HPV DNA 复制后，HPV 晚期基因表达被激活。最近的研究表明，DDR 因子还与 RNA 结合蛋白相互作用，并影响 RNA 加工。由 DNA 损伤激活并与 HPV DNA 结合的 DDR 因子可以招募剪接因子和 RNA 结合蛋白到 HPV DNA 上，并诱导 HPV 晚期基因表达。这种诱导是 HPV 信使 RNA（mRNA）可变多聚腺苷酸化和剪接改变的结果。HPV 利用 DDR 机制复制其 DNA 基因组，并在 RNA 加工水平上激活 HPV 晚期基因表达。
