目标：全球约有2.4亿人感染慢性乙型肝炎病毒（HBV），该病毒感染可能会进展为肝纤维化。HBV相关肝纤维化的机制尚未完全理解，且有效治疗方案很少。本研究旨在利用转录组学结合实验验证，鉴定用于治疗HBV相关肝纤维化的新靶点。 方法：收集了健康个体和慢性乙型肝炎患者的肝组织，共计5个。使用NovoMagic和Java GSEA筛选差异表达基因（DEGs）和关键基因。进行RNA测序数据中的免疫细胞浸润分析，并通过Western blotting（WB）、实时定量聚合酶链反应（RT-qPCR）和免疫组织化学证实结果。 结果：评估了1,105个差异表达基因，其中462个基因下调，643个基因上调​​。从DEGs中筛选出了关键基因，如肿瘤坏死因子（TNF）受体相关因子-2（TRAF2）。与健康对照组相比，TRAF2在患有乙型肝炎患者的肝纤维化中异常升高。肝纤维化程度和谷草转氨酶（ALT）、天门冬氨酸氨基转移酶（AST）和总胆红素（TBIL）血清水平与TRAF2表达呈正相关。TRAF2可能在控制T淋巴细胞介导的肝纤维化中起关键作用。结论：我们的发现表明，TRAF2对于HBV诱导的肝纤维化进展至关重要，并且可能是治疗乙型肝炎肝纤维化的有前途的靶点。版权所有©2023年Wu，Zhang，Wang，Zhang，Liu，Zhou，Chen，Wang，Peng和Fu。

Objectives: Approximately 240 million individuals are infected with chronic hepatitis B virus (HBV) worldwide. HBV infection can develop into liver fibrosis. The mechanism of HBV-related liver fibrosis has not been fully understood, and there are few effective treatment options. The goal of this study was to use transcriptomics in conjunction with experimental validation to identify new targets to treat HBV-related liver fibrosis. Methods: To identify differentially expressed genes (DEGs), five liver tissues were collected from both healthy individuals and patients with chronic hepatitis B. NovoMagic and Java GSEA were used to screen DEGs and key genes, respectively. Immunocell infiltration analysis of RNA-seq data was, and the results were confirmed by Western blotting (WB), real-time quantitative polymerase chain reaction (RT-qPCR), and immunohistochemistry. Results: We evaluated 1,105 genes with differential expression, and 462 and 643 genes showed down- and upregulation, respectively. The essential genes, such as tumor necrosis factor (TNF) receptor-associated factor-2 (TRAF2), were screened out of DEGs. TRAF2 expression was abnormally high in hepatic fibrosis in patients with hepatitis B compared with healthy controls. The degree of hepatic fibrosis and serum levels of glutamate transaminase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL) were positively linked with TRAF2 expression. TRAF2 may be crucial in controlling T lymphocyte-mediated liver fibrosis. Conclusion: Our findings imply that TRAF2 is essential for HBV-induced liver fibrosis progression, and it may potentially be a promising target for the treatment of hepatic fibrosis in hepatitis B.Copyright © 2023 Wu, Zhang, Wang, Zhang, Liu, Zhou, Chen, Wang, Peng and Fu.