研究表明，乙型肝炎病毒（HBV）相关的B细胞非霍奇金淋巴瘤（NHL）构成了一个具有独特临床特征的独特亚组。 HBV DNA 整合到 B 细胞基因组中是否是淋巴瘤发展的因果机制仍然是一个悬而未决的问题。使用基于杂交捕获的下一代测序和 RNA 测序，我们描述了 45 中 HBV 整合模式HBV相关B细胞NHL肿瘤组织。在13个样本（28.9%）中总共鉴定出354个HBV整合位点，表明B细胞NHL中整合频率相对较低。高血浆 HBV DNA 载量与 HBV 整合的存在无关。插入位点随机分布在所有淋巴瘤基因组中，无论在染色体水平还是在遗传水平上都没有任何优先热点。有趣的是，大多数 HBV 整合在 B 细胞 NHL 中是非克隆的，这意味着它们不会带来生存优势。对配对诊断-复发样本的分析表明，在疾病进展过程中 HBV 整合处于不稳定状态。此外，转录组分析揭示了 HBV 整合的有限生物学影响。我们的研究提供了 B 细胞 NHL 中无偏见的 HBV 整合图谱，揭示了 HBV DNA 整合在 B 细胞淋巴瘤发生中的微不足道的作用。© 2024。作者，获得施普林格自然有限公司的独家许可。

Studies have shown that hepatitis B virus (HBV)-associated B-cell non-Hodgkin lymphoma (NHL) constitutes a unique subgroup with distinct clinical features. It still leaves open the question of whether the integration of HBV DNA into the B-cell genome is a causal mechanism in the development of lymphoma.Using the hybridisation capture-based next generation sequencing and RNA sequencing, we characterised the HBV integration pattern in 45 HBV-associated B-cell NHL tumour tissues.A total of 354 HBV integration sites were identified in 13 (28.9%) samples, indicating the relatively low integration frequency in B-cell NHLs. High plasma HBV DNA loads were not associated with the existence of HBV integration. The insertion sites distributed randomly across all the lymphoma genome without any preferential hotspot neither at the chromosomal level nor at the genetic level. Intriguingly, most HBV integrations were nonclonal in B-cell NHLs, implying that they did not confer a survival advantage. Analysis of the paired diagnosis-relapse samples showed the unstable status of HBV integrations during disease progression. Furthermore, transcriptomic analysis revealed the limited biological impact of HBV integration.Our study provides an unbiased HBV integration map in B-cell NHLs, revealing the insignificant role of HBV DNA integration in B-cell lymphomagenesis.© 2024. The Author(s), under exclusive licence to Springer Nature Limited.