HPV16 and HPV18 type-specific APOBEC3 and integration profiles in different diagnostic categories of cervical samples

IF 4.7 Q1 VIROLOGY Tumour Virus Research Pub Date : 2021-12-01 DOI:10.1016/j.tvr.2021.200221
Sonja Lagström , Alexander Hesselberg Løvestad , Sinan Uğur Umu , Ole Herman Ambur , Mari Nygård , Trine B. Rounge , Irene Kraus Christiansen
{"title":"HPV16 and HPV18 type-specific APOBEC3 and integration profiles in different diagnostic categories of cervical samples","authors":"Sonja Lagström ,&nbsp;Alexander Hesselberg Løvestad ,&nbsp;Sinan Uğur Umu ,&nbsp;Ole Herman Ambur ,&nbsp;Mari Nygård ,&nbsp;Trine B. Rounge ,&nbsp;Irene Kraus Christiansen","doi":"10.1016/j.tvr.2021.200221","DOIUrl":null,"url":null,"abstract":"<div><p>Human papillomavirus (HPV) 16 and 18 are the most predominant types in cervical cancer. Only a small fraction of HPV infections progress to cancer, indicating that additional factors and genomic events contribute to the carcinogenesis, such as minor nucleotide variation caused by APOBEC3 and chromosomal integration.</p><p>We analysed intra-host minor nucleotide variants (MNVs) and integration in HPV16 and HPV18 positive cervical samples with different morphology. Samples were sequenced using an HPV whole genome sequencing protocol TaME-seq. A total of 80 HPV16 and 51 HPV18 positive samples passed the sequencing depth criteria of 300× reads, showing the following distribution: non-progressive disease (HPV16 n = 21, HPV18 n = 12); cervical intraepithelial neoplasia (CIN) grade 2 (HPV16 n = 27, HPV18 n = 9); CIN3/adenocarcinoma <em>in situ</em> (AIS) (HPV16 n = 27, HPV18 n = 30); cervical cancer (HPV16 n = 5).</p><p>Similar numbers of MNVs in HPV16 and HPV18 samples were observed for most viral genes, with the exception of HPV18 E4 with higher numbers across clinical categories. APOBEC3 signatures were observed in HPV16 lesions, while similar mutation patterns were not detected for HPV18. The proportion of samples with integration was 13% for HPV16 and 59% for HPV18 positive samples, with a noticeable portion located within or close to cancer-related genes.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":null,"pages":null},"PeriodicalIF":4.7000,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tvr.2021.200221","citationCount":"10","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tumour Virus Research","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2666679021000112","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"VIROLOGY","Score":null,"Total":0}
引用次数: 10

Abstract

Human papillomavirus (HPV) 16 and 18 are the most predominant types in cervical cancer. Only a small fraction of HPV infections progress to cancer, indicating that additional factors and genomic events contribute to the carcinogenesis, such as minor nucleotide variation caused by APOBEC3 and chromosomal integration.

We analysed intra-host minor nucleotide variants (MNVs) and integration in HPV16 and HPV18 positive cervical samples with different morphology. Samples were sequenced using an HPV whole genome sequencing protocol TaME-seq. A total of 80 HPV16 and 51 HPV18 positive samples passed the sequencing depth criteria of 300× reads, showing the following distribution: non-progressive disease (HPV16 n = 21, HPV18 n = 12); cervical intraepithelial neoplasia (CIN) grade 2 (HPV16 n = 27, HPV18 n = 9); CIN3/adenocarcinoma in situ (AIS) (HPV16 n = 27, HPV18 n = 30); cervical cancer (HPV16 n = 5).

Similar numbers of MNVs in HPV16 and HPV18 samples were observed for most viral genes, with the exception of HPV18 E4 with higher numbers across clinical categories. APOBEC3 signatures were observed in HPV16 lesions, while similar mutation patterns were not detected for HPV18. The proportion of samples with integration was 13% for HPV16 and 59% for HPV18 positive samples, with a noticeable portion located within or close to cancer-related genes.

Abstract Image

Abstract Image

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
不同诊断类别宫颈样本中HPV16和HPV18类型特异性APOBEC3及其整合谱
人乳头瘤病毒(HPV) 16和18是宫颈癌中最主要的类型。只有一小部分HPV感染进展为癌症,表明其他因素和基因组事件有助于致癌,如APOBEC3和染色体整合引起的小核苷酸变异。我们分析了不同形态的HPV16和HPV18阳性宫颈样本的宿主内小核苷酸变异(mnv)和整合。使用HPV全基因组测序方案TaME-seq对样本进行测序。共有80份HPV16和51份HPV18阳性样本通过了300x reads的测序深度标准,其分布如下:非进展性疾病(HPV16 n = 21, HPV18 n = 12);宫颈上皮内肿瘤(CIN) 2级(HPV16 n = 27, HPV18 n = 9);CIN3/原位腺癌(AIS) (HPV16 n = 27, HPV18 n = 30);在HPV16和HPV18样本中,大多数病毒基因的mnv数量相似,但HPV18 E4的mnv数量在临床类别中较高。在HPV16病变中观察到APOBEC3特征,而在HPV18病变中未检测到类似的突变模式。HPV16和HPV18阳性样本整合的比例分别为13%和59%,其中显著部分位于或接近癌症相关基因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
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
期刊最新文献
The imprint of viral oncoproteins on the variable clinical behavior among human papilloma virus-related oropharyngeal squamous cell carcinomas. Genomic diversity of HPV6 and HPV11 in recurrent respiratory papillomatosis: Association with malignant transformation in the lungs and clinical outcomes The SV40 virus enhancer functions as a somatic hypermutation-targeting element with potential tumorigenic activity Opportunities to advance cervical cancer prevention and care A new role for human papillomavirus 16 E2: Mitotic activation of the DNA damage response to promote viral genome segregation
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1