猪瘟（CSF）是由猪瘟病毒（CSFV）引起的，对生猪生产构成威胁。通过肿瘤坏死因子受体 (TNF-R) 相关因子 (TRAF) 等连接蛋白激活宿主先天免疫，对于诱导 NF-κB 通路至关重要。最近的研究揭示了线粒体抗病毒信号蛋白 (MAVS) 参与与 TRAF2、3、5 和 6 的相互作用，从而激活 NF-κB 和 IRF3 通路。这项研究表明，CSFV感染导致TRAF1 mRNA和蛋白水平上调；此外，TRAF1过表达抑制CSFV复制，而TRAF1敲低则促进复制，凸显了其在宿主对CSFV感染反应中的重要性。此外，在感染CSFV的PK-15细胞中检测到RIG-I、MAVS、TRAF1、IRF1和ISG15的表达，揭示TRAF1在RIG-I途径中发挥调节IRF1和ISG15的作用。此外，Co-IP、GST pull-down 和 IFA 分析表明，TRAF1 与 MAVS 相互作用，并在 CSFV 感染期间共定位于细胞质中。最终，TRAF1 作为 TRAF 家族的新成员，作为连接分子与 MAVS 结合，并在 RIG-I/MAVS 途径中作为 MAVS 下游的介质发挥作用，对抗 CSFV 复制。

Classical swine fever (CSF) is caused by the classical swine fever virus (CSFV), which poses a threat to swine production. The activation of host innate immunity through linker proteins such as tumor necrosis factor receptor (TNF-R)-associated factor (TRAF) is crucial for the induction of the NF-κB pathway. Recent research has revealed the involvement of mitochondrial antiviral-signaling protein (MAVS) in the interaction with TRAF2, 3, 5, and 6 to activate both the NF-κB and IRF3 pathways. This study revealed that CSFV infection led to the upregulation of TRAF1 mRNA and protein levels; moreover, TRAF1 overexpression inhibited CSFV replication, while TRAF1 knockdown promoted replication, highlighting its importance in the host response to CSFV infection. Additionally, the expression of RIG-I, MAVS, TRAF1, IRF1, and ISG15 were detected in PK-15 cells infected with CSFV, revealing that TRAF1 plays a role in regulating IRF1 and ISG15 within the RIG-I pathway. Furthermore, Co-IP, GST pull-down, and IFA analyses demonstrated that TRAF1 interacted with MAVS and co-localized in the cytoplasm during CSFV infection. Ultimately, TRAF1 acted as a novel member of the TRAF family, bound to MAVS as a linker molecule, and functioned as a mediator downstream of MAVS in the RIG-I/MAVS pathway against CSFV replication.