{"title":"好与坏:人类乳头瘤病毒对宿主DNA损伤反应的调节。","authors":"Caleb J Studstill, Cary A Moody","doi":"10.1146/annurev-virology-111821-103452","DOIUrl":null,"url":null,"abstract":"<p><p>High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.</p>","PeriodicalId":48761,"journal":{"name":"Annual Review of Virology","volume":" ","pages":"325-345"},"PeriodicalIF":8.1000,"publicationDate":"2023-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10956471/pdf/","citationCount":"0","resultStr":"{\"title\":\"For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.\",\"authors\":\"Caleb J Studstill, Cary A Moody\",\"doi\":\"10.1146/annurev-virology-111821-103452\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.</p>\",\"PeriodicalId\":48761,\"journal\":{\"name\":\"Annual Review of Virology\",\"volume\":\" \",\"pages\":\"325-345\"},\"PeriodicalIF\":8.1000,\"publicationDate\":\"2023-09-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10956471/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Annual Review of Virology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1146/annurev-virology-111821-103452\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2023/4/11 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"VIROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Annual Review of Virology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1146/annurev-virology-111821-103452","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/4/11 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"VIROLOGY","Score":null,"Total":0}
For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.
High-risk human papillomaviruses (HPVs) are associated with several human cancers. HPVs are small, DNA viruses that rely on host cell machinery for viral replication. The HPV life cycle takes place in the stratified epithelium, which is composed of different cell states, including terminally differentiating cells that are no longer active in the cell cycle. HPVs have evolved mechanisms to persist and replicate in the stratified epithelium by hijacking and modulating cellular pathways, including the DNA damage response (DDR). HPVs activate and exploit DDR pathways to promote viral replication, which in turn increases the susceptibility of the host cell to genomic instability and carcinogenesis. Here, we review recent advances in our understanding of the regulation of the host cell DDR by high-risk HPVs during the viral life cycle and discuss the potential cellular consequences of modulating DDR pathways.
期刊介绍:
The Annual Review of Virology serves as a conduit for disseminating thrilling advancements in our comprehension of viruses spanning animals, plants, bacteria, archaea, fungi, and protozoa. Its reviews illuminate novel concepts and trajectories in basic virology, elucidating viral disease mechanisms, exploring virus-host interactions, and scrutinizing cellular and immune responses to virus infection. These reviews underscore the exceptional capacity of viruses as potent probes for investigating cellular function.