Lumpy skin disease virus ORF142 protein inhibits type I interferon production by disrupting interactions of TBK1 and IRF3

Lumpy skin disease virus ORF142 protein inhibits type I interferon production by disrupting interactions of TBK1 and IRF3

Abstract Background Lumpy skin disease virus (LSDV) causes lumpy skin disease, which is one of the most devastating ruminant diseases. The pathogenesis of the disease remains largely unknown; however, the disease seriously threatens the global cattle-farming industry. In our previous study, we found...

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Bibliographic Details
Main Authors: Zihan Chen, Jingyu Wang, Baochun Lu, Heyu Li, Chuanli Liu, Huijuan Zeng, Jinping Chen, Shizhe Liu, Qifeng Jiang, Kun Jia
Format: Article
Language:English
Published: BMC 2025-04-01
Series:BMC Veterinary Research
Subjects:
LSDV
ORF142
IRF3
TBK1
Immune evasion
Online Access:https://doi.org/10.1186/s12917-025-04714-y
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Summary:Abstract Background Lumpy skin disease virus (LSDV) causes lumpy skin disease, which is one of the most devastating ruminant diseases. The pathogenesis of the disease remains largely unknown; however, the disease seriously threatens the global cattle-farming industry. In our previous study, we found that LSDV 142 gene deletion affected LSDV proliferation in cells and was an early gene involved in LSDV infection. Additionally, the study found that ORF142 inhibits the production of interferon beta. Results Herein, we report that LSDV inhibits the host antiviral response. The results revealed that the LSDV ORF142 protein inhibited interferon-promoter activation. ORF142 suppresses the host antiviral response by blocking interferon beta (IFN-β) production based on 381–417 amino acids at the C-terminal domain site of interferon regulatory factor 3 (IRF3). ORF142 interacts with IRF3 and interferes with the recruitment of IRF3 to TANK-binding kinase 1 (TBK1) in a dose-dependent manner, preventing nuclear translocation of IRF3. Conclusions These results suggest that LSDV ORF142 antagonizes host antiviral innate immunity by affecting the binding between TANK-binding kinase 1 and IRF3. Our findings provide new information regarding the pathogenesis of this virus.
ISSN:1746-6148

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