Interplay between the DNA damage response and the life cycle of DNA tumor viruses

IF 4.7 Q1 VIROLOGY
Caleb J. Studstill , Michelle Mac , Cary A. Moody
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引用次数: 0

Abstract

Approximately 20 % of human cancers are associated with virus infection. DNA tumor viruses can induce tumor formation in host cells by disrupting the cell's DNA replication and repair mechanisms. Specifically, these viruses interfere with the host cell's DNA damage response (DDR), which is a complex network of signaling pathways that is essential for maintaining the integrity of the genome. DNA tumor viruses can disrupt these pathways by expressing oncoproteins that mimic or inhibit various DDR components, thereby promoting genomic instability and tumorigenesis. Recent studies have highlighted the molecular mechanisms by which DNA tumor viruses interact with DDR components, as well as the ways in which these interactions contribute to viral replication and tumorigenesis. Understanding the interplay between DNA tumor viruses and the DDR pathway is critical for developing effective strategies to prevent and treat virally associated cancers. In this review, we discuss the current state of knowledge regarding the mechanisms by which human papillomavirus (HPV), merkel cell polyomavirus (MCPyV), Kaposi's sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV) interfere with DDR pathways to facilitate their respective life cycles, and the consequences of such interference on genomic stability and cancer development.

DNA损伤反应与DNA肿瘤病毒生命周期之间的相互作用。
大约20 % 许多人类癌症与病毒感染有关。DNA肿瘤病毒可以通过破坏细胞的DNA复制和修复机制来诱导宿主细胞中的肿瘤形成。具体来说,这些病毒会干扰宿主细胞的DNA损伤反应(DDR),DDR是一个复杂的信号通路网络,对维持基因组的完整性至关重要。DNA肿瘤病毒可以通过表达模拟或抑制各种DDR成分的癌蛋白来破坏这些途径,从而促进基因组的不稳定性和肿瘤发生。最近的研究强调了DNA肿瘤病毒与DDR成分相互作用的分子机制,以及这些相互作用促进病毒复制和肿瘤发生的方式。了解DNA肿瘤病毒和DDR途径之间的相互作用对于制定预防和治疗病毒相关癌症的有效策略至关重要。在这篇综述中,我们讨论了人类乳头瘤病毒(HPV)、默克尔细胞多瘤病毒(MCPyV)、卡波西肉瘤相关疱疹病毒(KSHV)和EB病毒(EBV)干扰DDR途径以促进其各自生命周期的机制,以及这种干扰对基因组稳定性和癌症发展的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Tumour Virus Research
Tumour Virus Research Medicine-Infectious Diseases
CiteScore
6.50
自引率
2.30%
发文量
16
审稿时长
56 days
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