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Newcastle Disease Virus V Protein Targets Phosphorylated STAT1 to Block IFN-I Signaling.
- Source :
-
PloS one [PLoS One] 2016 Feb 09; Vol. 11 (2), pp. e0148560. Date of Electronic Publication: 2016 Feb 09 (Print Publication: 2016). - Publication Year :
- 2016
-
Abstract
- Newcastle disease virus (NDV) V protein is considered as an effector for IFN antagonism, however, the mechanism remains unknown. In this study, the expression of STAT1 and phospho-STAT1 in cells infected with NDV or transfected with V protein-expressing plasmids were analyzed. Our results showed that NDV V protein targets phospho-STAT1 reduction in the cells depends on the stimulation of IFN-α. In addition, a V-deficient genotype VII recombinant NDV strain rZJ1-VS was constructed using reverse genetic technique to confirm the results. The rZJ1-VS lost the ability to reduce phospho-STAT1 and induced higher expression of IFN-responsive genes in infected cells. Furthermore, treatment with an ubiquitin E1 inhibitor PYR-41 demonstrated that phospho-STAT1 reduction was caused by degradation, but not de-phosphorylation. We conclude that NDV V protein targets phospho-STAT1 degradation to block IFN-α signaling, which adds novel knowledge to the strategies used by paramyxoviruses to evade IFN.
- Subjects :
- Animals
Cell Line
Chickens
Chlorocebus aethiops
Genes, Viral
Humans
Interferon-alpha metabolism
Mice
Mice, Inbred BALB C
Newcastle disease virus genetics
Phosphorylation
Protein Structure, Tertiary
Proteolysis
Recombination, Genetic
Signal Transduction
Vero Cells
Viral Proteins chemistry
Viral Proteins genetics
Interferon-alpha antagonists & inhibitors
Newcastle disease virus pathogenicity
Newcastle disease virus physiology
STAT1 Transcription Factor metabolism
Viral Proteins physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1932-6203
- Volume :
- 11
- Issue :
- 2
- Database :
- MEDLINE
- Journal :
- PloS one
- Publication Type :
- Academic Journal
- Accession number :
- 26859759
- Full Text :
- https://doi.org/10.1371/journal.pone.0148560