期刊
JOURNAL OF GENERAL VIROLOGY
卷 92, 期 -, 页码 2153-2159出版社
SOC GENERAL MICROBIOLOGY
DOI: 10.1099/vir.0.032987-0
关键词
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资金
- National Institute of Allergy and Infectious Diseases [P01 062885, N01-AI-30039, K22 (KAI074829A)]
- American Heart Association [SDG 0835151N]
- Parker Francis Foundation
Human respiratory syncytial virus (RSV), a leading cause of respiratory tract infections in infants, inhibits type I interferon (IFN)-dependent signalling, as well as IFN synthesis. RSV non-structural protein NS1 plays a significant role in this inhibition; however, the mechanism(s) responsible is not fully known. The transcription factor interferon regulatory factor (IRF)-3 is essential for viral-induced IFN-beta synthesis. In this study, we found that NS1 protein inhibits IRF-3-dependent gene transcription in constitutively active IRF-3 overexpressing cells, demonstrating that NS1 directly targets IRF-3. Our data also demonstrate that NS1 associates with IRF-3 and its transcriptional coactivator CBP, leading to disrupted association of IRF-3 to CBP and subsequent reduced binding of IRF-3 to the IEN-beta promoter without blocking viral-induced IRF-3 phosphorylation, nuclear translocation and dimerization, thereby identifying a novel molecular mechanism by which RSV inhibits IFN-beta synthesis.
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