The effects of hepatitis B virus integration into the genomes of hepatocellular carcinoma patients | Zendy

Zhaoshi Jiang | Zendy; Suchit Jhunjhunwala | Zendy; Jinfeng Liu | Zendy; Peter M. Haverty | Zendy; Michael Kennemer | Zendy; Yinghui Guan | Zendy; William Lee | Zendy; P. Carnevali | Zendy; Jeremy Stinson | Zendy; Stephanie L. Johnson | Zendy; Jingyu Diao | Zendy; Stacy Yeung | Zendy; A. A. Jubb | Zendy; Weilan Ye | Zendy; Thomas D. Wu | Zendy; Sharookh B. Kapadia | Zendy; Frédéric J. de Sauvage | Zendy; Robert Gentleman | Zendy; Howard M. Stern | Zendy; Somasekar Seshagiri | Zendy; Krishna Prasad Pant | Zendy; Zora Modrušan | Zendy; Dennis G. Ballinger | Zendy; Zemin Zhang | Zendy

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The effects of hepatitis B virus integration into the genomes of hepatocellular carcinoma patients

Author(s) -

Zhaoshi Jiang,

Suchit Jhunjhunwala,

Jinfeng Liu,

Peter M. Haverty,

Michael Kennemer,

Yinghui Guan,

William Lee,

P. Carnevali,

Jeremy Stinson,

Stephanie L. Johnson,

Jingyu Diao,

Stacy Yeung,

A. A. Jubb,

Weilan Ye,

Thomas D. Wu,

Sharookh B. Kapadia,

Frédéric J. de Sauvage,

Robert Gentleman,

Howard M. Stern,

Somasekar Seshagiri,

Krishna Prasad Pant,

Zora Modrušan,

Dennis G. Ballinger,

Zemin Zhang

Publication year - 2012

Publication title -

genome research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 9.556

H-Index - 297

eISSN - 1549-5469

pISSN - 1088-9051

DOI - 10.1101/gr.133926.111

Subject(s) - biology , hepatocellular carcinoma , hepatitis b virus , virology , genome , gene , hepatitis b , virus , transcriptome , genetics , gene expression

Hepatitis B virus (HBV) infection is a leading risk factor for hepatocellular carcinoma (HCC). HBV integration into the host genome has been reported, but its scale, impact and contribution to HCC development is not clear. Here, we sequenced the tumor and nontumor genomes (>80× coverage) and transcriptomes of four HCC patients and identified 255 HBV integration sites. Increased sequencing to 240× coverage revealed a proportionally higher number of integration sites. Clonal expansion of HBV-integrated hepatocytes was found specifically in tumor samples. We observe a diverse collection of genomic perturbations near viral integration sites, including direct gene disruption, viral promoter-driven human transcription, viral-human transcript fusion, and DNA copy number alteration. Thus, we report the most comprehensive characterization of HBV integration in hepatocellular carcinoma patients. Such widespread random viral integration will likely increase carcinogenic opportunities in HBV-infected individuals.

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