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标题: 全外显子组 HBV DNA 整合与 HBeAg 阴性慢性乙型肝炎肝内 HBV 储 [打印本页]

作者: StephenW    时间: 2021-11-9 08:39     标题: 全外显子组 HBV DNA 整合与 HBeAg 阴性慢性乙型肝炎肝内 HBV 储

全外显子组 HBV DNA 整合与 HBeAg 阴性慢性乙型肝炎肝内 HBV 储存库无关

    Valentina Svicher1、Romina Salpini1、Lorenzo Piermatteo1、Luca Carioti1、Arianna Battisti1,2、Luna Colagrossi1,3、Rossana Scutari1、Matteo Surdo4、Valeria Cacciafesta4、Andrea Nuccitelli4、Navjyot Hansi2、Francesca Ceckarerin Up、Francesca Cecerstein、Fed Caro ://orcid.org/0000-0001-9201-0094Patrick TF Kennedy2

    与 Patrick T F Kennedy 博士的通信,Barts 肝脏中心,免疫生物学,Blizard 研究所,Barts 和伦敦医学与牙科学院,伦敦玛丽皇后大学,Newark Street,London,E1 2AT,UK; [email protected]

抽象的

目的 HBV DNA 整合在促进肝癌发生中的作用以及肝内 HBV 储库调节肝病进展的程度仍知之甚少。我们检查了肝内 HBV 储存库、HBV DNA 整合的发生及其对乙型肝炎‘e’抗原 (HBeAg) 阴性慢性乙型肝炎 (CHB) 肝细胞转录组的影响。

设计 分析了 84 名 HBeAg 阴性 CHB 患者的肝组织,其中低 (n=12)、中度 (n=25) 和高 (n=47) 血清 HBV DNA。共价闭合环状 DNA (cccDNA)、前基因组 RNA (pgRNA) 通过定量 PCR 进行评估,全外显子组和转录组测序由 Illumina 进行,HBV DNA 整合的负荷通过数字液滴 PCR 进行评估。

结果 低、中度血清HBV DNA患者肝内cccDNA和pgRNA表现出可比性,显着低于高HBV DNA患者,而乙肝核心相关抗原与肝内HBV储库密切相关,反映了cccDNA的数量。在大量患者中检测到全外显子组整合(高、中和低病毒血症患者分别为 55.6%、14.3% 和 25%),频率范围为 0.5 至 157 次整合/1000 个肝细胞。乙型肝炎表面抗原 >5000 IU/mL 预测外显子组内的整合,这些整合定位于涉及肝癌发生、脂质/药物代谢调节和抗病毒/炎症反应的基因中。 HBV DNA 整合患者的特定基因(包括原癌基因 hRAS)的转录水平较高,支持低至中度病毒血症患者的潜在致癌风险。

结论 HBV DNA 整合发生在所有 HBeAg 阴性 CHB 患者中,包括那些 HBV 储库有限的患者;定位于参与致癌作用的基因并改变肝细胞转录组。
数据可用性声明

可应合理要求提供数据。与研究相关的所有数据都包含在文章中或作为补充信息上传。所有临床数据都收集在一个匿名数据库中,该数据库可在 The Blizard Institute, Barts 和 The London SMD, QMUL 获得。负责人:PTF
http://creativecommons.org/licenses/by-nc/4.0/

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http://dx.doi.org/10.1136/gutjnl-2020-323300
作者: StephenW    时间: 2021-11-9 08:39

Whole exome HBV DNA integration is independent of the intrahepatic HBV reservoir in HBeAg-negative chronic hepatitis B

    Valentina Svicher1, Romina Salpini1, Lorenzo Piermatteo1, Luca Carioti1, Arianna Battisti1,2, Luna Colagrossi1,3, Rossana Scutari1, Matteo Surdo4, Valeria Cacciafesta4, Andrea Nuccitelli4, Navjyot Hansi2, Francesca Ceccherini Silberstein1, Carlo Federico Perno5, Upkar S Gill2, http://orcid.org/0000-0001-9201-0094Patrick T F Kennedy2

    Correspondence to Dr Patrick T F Kennedy, Barts Liver Centre, Immunobiology, Blizard Institute, Barts and The London School of Medicine & Dentistry, Queen Mary University of London, Newark Street, London, E1 2AT, UK; [email protected]

Abstract

Objective The involvement of HBV DNA integration in promoting hepatocarcinogenesis and the extent to which the intrahepatic HBV reservoir modulates liver disease progression remains poorly understood. We examined the intrahepatic HBV reservoir, the occurrence of HBV DNA integration and its impact on the hepatocyte transcriptome in hepatitis B ‘e’ antigen (HBeAg)-negative chronic hepatitis B (CHB).

Design Liver tissue from 84 HBeAg-negative patients with CHB with low (n=12), moderate (n=25) and high (n=47) serum HBV DNA was analysed. Covalently closed circular DNA (cccDNA), pregenomic RNA (pgRNA) were evaluated by quantitative PCR, whole exome and transcriptome sequencing was performed by Illumina, and the burden of HBV DNA integrations was evaluated by digital droplet PCR.

Results Patients with low and moderate serum HBV DNA displayed comparable intrahepatic cccDNA and pgRNA, significantly lower than in patients with high HBV DNA, while hepatitis B core-related antigen correlated strongly with the intrahepatic HBV reservoir, reflecting cccDNA quantity. Whole exome integration was detected in a significant number of patients (55.6%, 14.3% and 25% in high, moderate and low viraemic patients, respectively), at a frequency ranging from 0.5 to 157 integrations/1000 hepatocytes. Hepatitis B surface antigen >5000 IU/mL predicted integration within the exome and these integrations localised in genes involved in hepatocarcinogenesis, regulation of lipid/drug metabolism and antiviral/inflammatory responses. Transcript levels of specific genes, including the proto-oncogene hRAS, were higher in patients with HBV DNA integration, supporting an underlying oncogenic risk in patients with low-level to moderate-level viraemia.

Conclusions HBV DNA integration occurs across all HBeAg-negative patients with CHB, including those with a limited HBV reservoir; localising in genes involved in carcinogenesis and altering the hepatocyte transcriptome.
Data availability statement

Data are available on reasonable request. All data relevant to the study are included in the article or uploaded as supplementary information. All clinical data have been collected in an anonymous database available at The Blizard Institute, Barts and The London SMD, QMUL. Responsible: PTFK
http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

http://dx.doi.org/10.1136/gutjnl-2020-323300

作者: StephenW    时间: 2021-11-9 08:40

https://gut.bmj.com/content/gutjnl/70/12/2337.full.pdf
作者: zjs123    时间: 2021-11-9 14:32

请问这篇文章的意思是 所有e抗原阴性的患者都有HBV基因整合,还是hbsag>5000 iu的才会发生整合
作者: StephenW    时间: 2021-11-9 15:07

回复 zjs123 的帖子

所有e抗原阴性的患者, HBV DNA 整合率:
高病毒 55.6%
中病毒 14.3%
低病毒 25%

hbsag>5000 iu/ml 可以预测HBeAg 阴性患者的 HBV DNA 整合事件.


作者: zjs123    时间: 2021-11-9 15:38

谢谢你的回复。我的hbsag接近20,000 IU, 肯定是发生整合了。现在对我的未来很担忧啊
作者: StephenW    时间: 2021-11-9 16:57

回复 zjs123 的帖子

HBV DNA 整合不会自动导致癌症 , 但会增加风险 , 因此建议每半年检查一次 AFP + 超声波 .
作者: zjs123    时间: 2021-11-9 19:56

谢谢你的回复,我会定期按时检查




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