河南农业科学 ›› 2021, Vol. 50 ›› Issue (12): 1-9.DOI: 10.15933/j.cnki.1004-3268.2021.12.001

• 综述 • 上一篇    下一篇

DNA 病毒基因组复制与宿主细胞DDR 信号网络互作的研究进展

王平利,夏璐,魏战勇   

  1. (河南农业大学动物医学院,河南郑州450046)
  • 收稿日期:2021-08-23 出版日期:2021-12-15 发布日期:2022-01-28
  • 通讯作者: 魏战勇(1975-),男,河南安阳人,教授,博士,主要从事动物分子病毒学、分子免疫学研究。E-mail:weizhanyong@henau.edu.cn
  • 作者简介:王平利(1976-),女,河南濮阳人,讲师,硕士,主要从事动物病毒病病理研究。E-mail:1175913146@ qq.com
  • 基金资助:
    国家自然科学基金面上项目(31772722);河南省高等学校重点科研项目(18A230001)

Advances in the Interaction between DNA Viruses Genome Replication and Host Cellular DDR Signal Networks

WANG Pingli,XIA Lu,WEI Zhanyong   

  1. (College of Veterinary Medicine,Henan Agricultural University,Zhengzhou 450046,China)
  • Received:2021-08-23 Published:2021-12-15 Online:2022-01-28

摘要: DNA病毒基因组的编码能力有限,在其基因组复制过程中与细胞内的DNA损伤反应(DDR)信号网络发生复杂广泛的相互作用,创造利于病毒复制的细胞内环境。MRN 复合物(MRE11‐RAD50‐NBS1)、复制蛋白A(RPA)分别识别DNA双链断裂(DSB)和单链断裂(SSB)。DNA病毒选择性地激活磷脂酰肌醇-3激酶样激酶(PI3KK)ATM(Ataxia telangiectasia mutated)、ATR(Ataxia telangiectasia and Rad3 related)或DNA-PKcs(DNA‐dependent protein kinase catalytic subunit),通过调控细胞周期进展、启动非同源末端连接(NHEJ)和同源重组修复(HRR)等不同的DNA修复途径,选择性地激活利用或抑制降解宿主细胞DDR组分来完成其感染周期,表现在病毒复制中心(VRC)处募集结合了不同的参与细胞DNA损伤和修复的蛋白质。综述了DNA病毒复制与宿主细胞DDR信号网络的互作机制,旨在为研究DNA病毒的复制和致病分子机制提供思路。

关键词: DNA病毒, 基因组复制, DNA损伤反应, 病毒复制中心, 分子机制

Abstract: The genomes of DNA viruses have limited encoding capabilities.They create intracellular environment conducive to viral replication through complex and extensive interaction with cellular DNA damage response(DDR)signal networks during their genomes replication. MRN(MRE11‐RAD50‐NBS1)and RPA(replication protein A) specifically detect damaged DNA by respectively interacting with double‐strand break(DSB)and single‐strand break(SSB).DNA viruses selectively activate at least one of the three phosphatidylinositol‐3‐kinase‐like kinases(PI3KK),ataxia telangiectasia mutated(ATM),ataxia telangiectasia and Rad3 related(ATR),and DNA‐dependent protein kinase catalytic subunit(DNA‐PKcs) to manipulate cellular cycles and trigger two main types of DNA repairments:non‐homologous end joining(NHEJ)and homologous recombination repair(HRR).In order to complete their productive infection cycles,DNA viruses selectively activate or degrade host cellular DDR components.The viral replication center(VRC)recruits plenty of different proteins involved in cellular DDR.The interaction mechanism between replication of DNA viruses and host cellular DDR signa networks was reviewed to provide ideas for exploring the molecular mechanisms of DNA viruses replication and pathogenesis.

Key words: DNA virus, Genome replication, DDR, VRC, Molecular mechanism

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