...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Genomics >The role of DNA repair in herpesvirus pathogenesis
【24h】

The role of DNA repair in herpesvirus pathogenesis

机译：DNA修复在疱疹病毒发病机理中的作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

In cells latently infected with a herpesvirus, the viral DNA is present in the cell nucleus, but it is not extensively replicated or transcribed. In this suppressed state the virus DNA is vulnerable to mutagenic events that affect the host cell and have the potential to destroy the virus' genetic integrity. Despite the potential for genetic damage, however, herpesvirus sequences are well conserved after reactivation from latency. To account for this apparent paradox, I have tested the idea that host cell-encoded mechanisms of DNA repair are able to control genetic damage to latent herpesviruses. Studies were focused on homologous recombination-dependent DNA repair (HR). Methods of DNA sequence analysis were employed to scan herpesvirus genomes for DNA features able to activate HR. Analyses were carried out with a total of 39 herpesvirus DNA sequences, a group that included viruses from the alpha-, beta- and gamma-subfamilies. The results showed that all 39 genome sequences were enriched in two or more of the eight recombination-initiating features examined. The results were interpreted to indicate that HR can stabilize latent herpesvirus genomes. The results also showed, unexpectedly, that repair-initiating DNA features differed in alpha- compared to gamma-herpesviruses. Whereas inverted and tandem repeats predominated in alpha-herpesviruses, gamma-herpesviruses were enriched in short, GC-rich initiation sequences such as CCCAG and depleted in repeats. In alpha-herpesviruses, repair-initiating repeat sequences were found to be concentrated in a specific region (the S segment) of the genome while repair-initiating short sequences were distributed more uniformly in gamma-herpesviruses. The results suggest that repair pathways are activated differently in alpha- compared to gamma-herpesviruses. (C) 2014 The Author. Published by Elsevier Inc.
机译：在被疱疹病毒潜伏感染的细胞中，病毒DNA存在于细胞核中，但并未大量复制或转录。在这种抑制状态下，病毒DNA容易受到诱变事件的影响，这些事件会影响宿主细胞，并有可能破坏病毒的遗传完整性。尽管存在遗传损伤的可能性，但是从潜伏期重新激活后，疱疹病毒序列仍被很好地保守。为了解决这个明显的矛盾，我测试了一种想法，即宿主细胞编码的DNA修复机制能够控制对潜伏性疱疹病毒的遗传损伤。研究集中在同源重组依赖的DNA修复（HR）。 DNA序列分析的方法被用来扫描疱疹病毒基因组中能够激活HR的DNA特征。用总共39条疱疹病毒DNA序列进行了分析，其中包括来自α，β和γ亚家族的病毒。结果表明，所有39个基因组序列均富集了所检查的8个重组起始特征中的2个或更多。结果被解释为表明HR可以稳定潜在的疱疹病毒基因组。结果也出乎意料地表明，与γ-疱疹病毒相比，修复启动DNA的特征在α-方面有所不同。反向和串联重复在α-疱疹病毒中占优势，而γ-疱疹病毒则富含短而富含GC的起始序列（如CCCAG），而重复序列却被耗尽。在α-疱疹病毒中，发现修复启动的重复序列集中在基因组的特定区域（S片段），而修复启动的短序列在γ-疱疹病毒中分布更均匀。结果表明，与γ-疱疹病毒相比，修复途径在α-中的激活方式有所不同。 （C）2014作者。由Elsevier Inc.发布

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号