乳头瘤病毒潜伏期的生物学。

The Open Virology Journal Pub Date : 2012-01-01 Epub Date: 2012-12-28 DOI:10.2174/1874357901206010190
Gareth Adam Maglennon, John Doorbar
{"title":"乳头瘤病毒潜伏期的生物学。","authors":"Gareth Adam Maglennon, John Doorbar","doi":"10.2174/1874357901206010190","DOIUrl":null,"url":null,"abstract":"<p><p>The presence of viral DNA in the absence of disease has suggested that papillomaviruses, like many other viruses, can exist as latent infections in the skin or other epithelial sites. In animal models, where detailed investigation has been carried out, papillomavirus DNA can be found at sites of previous infection following immune regression, with the site of latent infection being the epithelial basal layer. Such studies suggest that immune surveillance can restrict viral gene expression in the basal and parabasal layers without efficiently suppressing viral genome replication, most probably through the action of memory T-cells in the skin or dermis. Although gradual papillomavirus genome loss appears to occur over time at latent sites, immunosuppression can arrest this, and can lead to an elevation in viral genome copy number in experimental systems. In addition to immune-mediated latency, it appears that a similar situation can be achieved following infection at low virus titres and/or infection at epithelial sites where the virus life cycle is not properly supported. Such silent of asymptomatic infections do not necessarily involve the host immune system and may be controlled by different mechanisms. It appears that virus reactivation can be triggered by mechanical irritation, wounding or by UV irradiation which changes the local environment. Although the duration of papillomavirus latency in humans is not yet known, it is likely that some of the basic principles will resemble those elucidated in these model systems, and that persistence in the absence of disease may be the default outcome for at least some period of time following regression.</p>","PeriodicalId":23111,"journal":{"name":"The Open Virology Journal","volume":"6 ","pages":"190-7"},"PeriodicalIF":0.0000,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c7/30/TOVJ-6-190.PMC3547330.pdf","citationCount":"0","resultStr":"{\"title\":\"The biology of papillomavirus latency.\",\"authors\":\"Gareth Adam Maglennon, John Doorbar\",\"doi\":\"10.2174/1874357901206010190\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The presence of viral DNA in the absence of disease has suggested that papillomaviruses, like many other viruses, can exist as latent infections in the skin or other epithelial sites. In animal models, where detailed investigation has been carried out, papillomavirus DNA can be found at sites of previous infection following immune regression, with the site of latent infection being the epithelial basal layer. Such studies suggest that immune surveillance can restrict viral gene expression in the basal and parabasal layers without efficiently suppressing viral genome replication, most probably through the action of memory T-cells in the skin or dermis. Although gradual papillomavirus genome loss appears to occur over time at latent sites, immunosuppression can arrest this, and can lead to an elevation in viral genome copy number in experimental systems. In addition to immune-mediated latency, it appears that a similar situation can be achieved following infection at low virus titres and/or infection at epithelial sites where the virus life cycle is not properly supported. Such silent of asymptomatic infections do not necessarily involve the host immune system and may be controlled by different mechanisms. It appears that virus reactivation can be triggered by mechanical irritation, wounding or by UV irradiation which changes the local environment. Although the duration of papillomavirus latency in humans is not yet known, it is likely that some of the basic principles will resemble those elucidated in these model systems, and that persistence in the absence of disease may be the default outcome for at least some period of time following regression.</p>\",\"PeriodicalId\":23111,\"journal\":{\"name\":\"The Open Virology Journal\",\"volume\":\"6 \",\"pages\":\"190-7\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c7/30/TOVJ-6-190.PMC3547330.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Open Virology Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/1874357901206010190\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2012/12/28 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Open Virology Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1874357901206010190","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/12/28 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

在没有疾病的情况下病毒DNA的存在表明,乳头瘤病毒和许多其他病毒一样,可以作为潜伏感染存在于皮肤或其他上皮部位。在进行了详细研究的动物模型中,在免疫消退后,可以在先前感染的部位发现乳头瘤病毒DNA,潜在感染的部位是上皮基底层。这些研究表明,免疫监测可以限制病毒基因在基底层和副基底层的表达,而不会有效抑制病毒基因组复制,很可能是通过皮肤或真皮中记忆T细胞的作用。尽管随着时间的推移,乳头瘤病毒基因组在潜伏位点似乎会逐渐丢失,但免疫抑制可以阻止这种情况,并可能导致实验系统中病毒基因组拷贝数的增加。除了免疫介导的潜伏期外,在低病毒滴度感染和/或在病毒生命周期没有得到适当支持的上皮部位感染后,似乎也可以实现类似的情况。这种无症状感染的沉默不一定涉及宿主免疫系统,可能受到不同机制的控制。看来,病毒的重新激活可能是由机械刺激、伤害或紫外线照射引起的,紫外线照射会改变局部环境。尽管人类乳头瘤病毒潜伏时间尚不清楚,但一些基本原理可能与这些模型系统中阐明的原理相似,并且在没有疾病的情况下持续存在可能是回归后至少一段时间的默认结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The biology of papillomavirus latency.

The biology of papillomavirus latency.

The biology of papillomavirus latency.

The presence of viral DNA in the absence of disease has suggested that papillomaviruses, like many other viruses, can exist as latent infections in the skin or other epithelial sites. In animal models, where detailed investigation has been carried out, papillomavirus DNA can be found at sites of previous infection following immune regression, with the site of latent infection being the epithelial basal layer. Such studies suggest that immune surveillance can restrict viral gene expression in the basal and parabasal layers without efficiently suppressing viral genome replication, most probably through the action of memory T-cells in the skin or dermis. Although gradual papillomavirus genome loss appears to occur over time at latent sites, immunosuppression can arrest this, and can lead to an elevation in viral genome copy number in experimental systems. In addition to immune-mediated latency, it appears that a similar situation can be achieved following infection at low virus titres and/or infection at epithelial sites where the virus life cycle is not properly supported. Such silent of asymptomatic infections do not necessarily involve the host immune system and may be controlled by different mechanisms. It appears that virus reactivation can be triggered by mechanical irritation, wounding or by UV irradiation which changes the local environment. Although the duration of papillomavirus latency in humans is not yet known, it is likely that some of the basic principles will resemble those elucidated in these model systems, and that persistence in the absence of disease may be the default outcome for at least some period of time following regression.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信