为了研究乙型肝炎病毒（HBV）在肝癌基因组整合，我们针对81 HBV阳性和7 HBV阴性的肝细胞癌（肝癌）和癌旁正常组织进行了大规模并行测序。我们发现与癌旁组织相比（30.7％），HBV 整合在肿瘤（86.4％）组织中更常出现。在HBV断点位置拷贝数变异（CNVs）显着增加，可能诱发染色体不稳定。约40％的HBV基因组内的HBV断点分别位于由构成的HBV基因组1,800 bp的区域中。我们还明确了经常性的整合事件（在4例HCC），就是公认的与癌症相关的TERT，MLL4和CCNE1基因在肿瘤组织中表达上调，并由RNA测序（RNA-seq的）和Sanger测序得到了验证。我们还发现HBV整合的数量与患者的生存期相关。　　To survey hepatitis B virus (HBV) integration in liver cancer genomes, we conducted massively parallel sequencing of 81 HBV-positive and 7 HBV-negative hepatocellular carcinomas (HCCs) and adjacent normal tissues. We found that HBV integration is observed more frequently in the tumors (86.4%) than in adjacent liver tissues (30.7%). Copy-number variations (CNVs) were significantly increased at HBV breakpoint locations where chromosomal instability was likely induced. Approximately 40% of HBV breakpoints within the HBV genome were located within a 1,800-bp region where the viral enhancer, X gene and core gene are located. We also identified recurrent HBV integration events (in *4 HCCs) that were validated by RNA sequencing (RNA-seq) and Sanger sequencing at the known and putative cancer-related TERT, MLL4 and CCNE1 genes, which showed upregulated gene expression in tumor versus normal tissue. We also report evidence that suggests that the number of HBV integrations is associated with patient survival.