期刊
FRONTIERS IN MICROBIOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2021.761282
关键词
pseudorabies virus; US3 protein; innate immunity; IRF3; IFN-beta
类别
资金
- Young Talent of SEAC [(2018)98]
- Fundamental Research Funds for the Central Universities [31920190003, 31920200003, 31920210051]
- Open Funds of the Biomedical Research Center from Northwest Minzu University [EB201801]
- Gansu Youth Science and Technology Fund Project [20JR5RA501]
The US3 protein of pseudorabies virus has been identified as a crucial viral factor that represses interferon beta expression by targeting interferon regulatory factor 3. This study reveals a novel strategy used by PRV to inhibit IFN-beta production and evade host innate immunity.
Pseudorabies virus is a typical swine alphaherpesvirus, which can cause obvious neurological disorders and reproductive failure in pigs. It is capable of evading host antiviral immune response. However, the mechanism by which many PRV proteins assist the virus to evade innate immunity is not fully understood. This study identified PRV US3 protein as a crucial antagonistic viral factor that represses interferon beta (IFN-beta) expression. A in-depth study showed that US3 protein restricted type I IFN production by targeting interferon regulatory factor 3 (IRF3), a key molecule required for type I IFN induction. Additionally, US3 protein interacted with IRF3, degraded its protein expression to block the phosphorylation of IRF3. These findings suggested a novel strategy utilized by PRV to inhibit IFN-beta production and escape the host innate immunity.
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