ArticleJournal of virology2010
Role of interferon antagonist activity of rabies virus phosphoprotein in viral pathogenicity.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 92 citations in OpenAlex.
- Hendra virus genotypes 1 and 2 differ in V protein-mediated immune evasion.The Journal of general virology · 2026Article
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- Structural insights into the multifunctionality of rabies virus P3 protein.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Substitution of S179P in the Lyssavirus Phosphoprotein Impairs Its Interferon Antagonistic Function.Journal of virology · 2022Article
- Establishment of a reverse genetics system for rabies virus strain Komatsugawa.The Journal of veterinary medical science · 2022Article
- Lyssavirus P Protein Isoforms Diverge Significantly in Subcellular Interactions Underlying Mechanisms of Interferon Antagonism.Journal of virology · 2022Article
- Regulation of innate immune responses by rabies virus.Animal models and experimental medicine · 2022Review
- Deactivation of the antiviral state by rabies virus through targeting and accumulation of persistently phosphorylated STAT1.PLoS pathogens · 2022Article
- Reduced IFN-ß inhibitory activity of Lagos bat virus phosphoproteins in human compared to Eidolon helvum bat cells.PloS one · 2022Article
- Bimolecular Fluorescence Complementation: Quantitative Analysis of In Cell Interaction of Nuclear Transporter Importin α with Cargo Proteins.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Innate Immune Signaling and Role of Glial Cells in Herpes Simplex Virus- and Rabies Virus-Induced Encephalitis.Viruses · 2021Review
- The Ebola Virus Interferon Antagonist VP24 Undergoes Active Nucleocytoplasmic Trafficking.Viruses · 2021Article
- SARS-CoV-2 suppresses IFNβ production mediated by NSP1, 5, 6, 15, ORF6 and ORF7b but does not suppress the effects of added interferon.PLoS pathogens · 2021Article
- Definition of the immune evasion-replication interface of rabies virus P protein.PLoS pathogens · 2021Article
- Phenotypic Divergence of P Proteins of Australian Bat Lyssavirus Lineages Circulating in Microbats and Flying Foxes.Viruses · 2021Article
- Antivirals that target the host IMPα/β1-virus interface.Biochemical Society transactions · 2021Review
- Naturally occurring substitution in one amino acid in VHSV phosphoprotein enhances viral virulence in flounder.PLoS pathogens · 2021Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
- Lyssavirus P-protein selectively targets STAT3-STAT1 heterodimers to modulate cytokine signalling.PLoS pathogens · 2020Article
- Genetic and Phenotypic Characterization of a Rabies Virus Strain Isolated from a Dog in Tokyo, Japan in the 1940s.Viruses · 2020Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fixed rabies virus (RV) strain Nishigahara kills adult mice after intracerebral inoculation, whereas the chicken embryo fibroblast cell-adapted strain Ni-CE causes nonlethal infection in adult mice. We previously reported that the chimeric CE(NiP) strain, which has the phosphoprotein (P protein) gene from the Nishigahara strain in the genetic background of the Ni-CE strain, causes lethal infection in adult mice, indicating that the P gene is responsible for the different pathogenicities of the Nishigahara and Ni-CE strains. Previous studies demonstrated that RV P protein binds to the interferon (IFN)-activated transcription factor STAT1 and blocks IFN signaling by preventing its translocation to the nucleus. In this study, we examine the molecular mechanism by which RV P protein determines viral pathogenicity by comparing the IFN antagonist activities of the Nishigahara and Ni-CE P proteins. The results, obtained from both RV-infected cells and cells transfected to express P protein only, show that Ni-CE P protein is significantly impaired for its capacity to block IFN-activated STAT1 nuclear translocation and, consequently, inhibits IFN signaling less efficiently than Nishigahara P protein. Further, it was demonstrated that a defect in the nuclear export of Ni-CE P protein correlates with a defect in its ability to cause the mislocalization of STAT1. These data provide the first evidence that the capacity of the RV P protein to inhibit STAT1 nuclear translocation and IFN signaling correlates with the viral pathogenicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.