|
DVID
|
1019586 |
|
VISID
|
TVIS10015441 |
|
Chromosome
|
chr11 |
|
GRCh38 Location
|
49728425 |
|
Disease
|
Carcinoma, Hepatocellular |
|
Sample
|
Tumor |
|
Virus Reference Genome
|
AB014381.1 |
|
Target Gene
|
GRM5P1 |
Literature Information
|
PubMed PMID
|
23867110
|
|
Year
|
2013 Oct;102(4):338-44 |
|
Journal
|
Genomics |
|
Title
|
HIVID: an efficient method to detect HBV integration using low coverage sequencing. |
|
Author
|
Li W,Zeng X,Lee NP,Liu X,Chen S,Guo B,Yi S,Zhuang X,Chen F,Wang G,Poon RT,Fan ST,Mao M,Li Y,Li S,Wang J,Jianwang,Xu X,Jiang H,Zhang X |
|
Evidence
|
We reported HIVID (high-throughput Viral Integration Detection), a novel experimental and computational method to detect the location of Hepatitis B Virus (HBV) integration breakpoints in Hepatocellular Carcinoma (HCC) genome. In this method, the fragments with HBV sequence were enriched by a set of HBV probes and then processed to high-throughput sequencing. In order to evaluate the performance of HIVID, we compared the results of HIVID with that of whole genome sequencing method (WGS) in 28 HCC tumors. We detected a total of 246 HBV integration breakpoints in HCC genome, 113 out of which were within 400bp upstream or downstream of 125 breakpoints identified by WGS method, covering 89.3% (125/140) of total breakpoints. The integration was located in the gene TERT, MLL4, and CCNE1. In addition, we discovered 133 novel breakpoints missed by WGS method, with 66.7% (10/15) of validation rate. Our study shows HIVID is a cost-effective methodology with high specificity and sensitivity to identify viral integration in human genome.
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