期刊
VIROLOGY JOURNAL
卷 8, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1743-422X-8-48
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资金
- Austrian Science Fund (FWF) [P20080-Med]
- Salzburg Research Fellowship [P147200-06]
- Salzburg University [SF0706V]
- Austrian Science Fund (FWF) [P20080] Funding Source: Austrian Science Fund (FWF)
The nonstructural proteins 1 (NS1) from influenza A and B viruses are known as the main viral factors antagonising the cellular interferon (IFN) response, inter alia by inhibiting the retinoic acid-inducible gene I (RIG-I) signalling. The cytosolic pattern-recognition receptor RIG-I senses double-stranded RNA and 5'-triphosphate RNA produced during RNA virus infections. Binding to these ligands activates RIG-I and in turn the IFN signalling. We now report that the influenza C virus NS1 protein also inhibits the RIG-I-mediated IFN signalling. Employing luciferase-reporter assays, we show that expression of NS1-C proteins of virus strains C/JJ/50 and C/JHB/1/66 considerably reduced the IFN-beta promoter activity. Mapping of the regions from NS1-C of both strains involved in IFN-beta promoter inhibition showed that the N-terminal 49 amino acids are dispensable, while the C-terminus is required for proper modulation of the IFN response. When a mutant RIG-I, which is constitutively active without ligand binding, was employed, NS1-C still inhibited the downstream signalling, indicating that IFN inhibitory properties of NS1-C are not necessarily linked to an RNA binding mechanism.
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