Uncovering the Interaction between TRAF1 and MAVS in the RIG-I Pathway to Enhance the Upregulation of IRF1/ISG15 during Classical Swine Fever Virus Infection

被引：0

作者：

Zhang, Liyuan ^{[1
,2
]}

Tang, Rongze ^{[1
,2
]}

Liang, Dongli ^{[1
,2
]}

Wang, Wenfeng ^{[1
,2
]}

Min, Kaijun ^{[1
,2
]}

Luo, Tingrong ^{[1
,2
,3
,4
]}

Li, Xiaoning ^{[1
,2
,3
,4
]}

机构：

[1] Guangxi Univ, Coll Anim Sci & Vet Med, Nanning 530004, Peoples R China

[2] Guangxi Univ, State Key Lab Conservat & Utilizat Subtrop Agrobio, Nanning 530004, Peoples R China

[3] Guaxi Zhuang Autonomous Reg Engn Res Ctr Vet Biol, Nanning 530004, Peoples R China

[4] Guangxi Key Lab Anim Breeding Dis Control & Preven, Nanning 530004, Peoples R China

来源：

CELLS | 2024年 / 13卷 / 13期

基金：

中国国家自然科学基金;

关键词：

CSFV (classical swine fever virus); TRAF1 (tumor necrosis factor receptor (TNF-R)-associated factor 1); RIG-I (retinoic acid-inducible gene I); MAVS (mitochondrial antiviral-signaling protein); IRF1 (interferon regulatory factor 1); ISG15 (interferon-stimulating gene 15); NF-KAPPA-B; PHOSPHORYLATION; MECHANISMS; EXPRESSION; BINDING; PROTEIN; IMMUNE;

D O I：

10.3390/cells13131165

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

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-kappa B 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-kappa B 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.

引用

页数：17