ArticlePLoS pathogens2020
Lyssavirus P-protein selectively targets STAT3-STAT1 heterodimers to modulate cytokine signalling.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Hendra virus genotypes 1 and 2 differ in V protein-mediated immune evasion.The Journal of general virology · 2026Article
- Human brain cell types shape host-rabies virus transcriptional interactions revealing a preexisting pro-viral astrocyte subpopulation.Cell reports · 2025Article
- Article
- Activation of HTR2B Suppresses Osteosarcoma Progression through the STAT1-NLRP3 Inflammasome Pathway and Promotes OASL1+ Macrophage Production to Enhance Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- IRF2 Cooperates with Phosphoprotein of Spring Viremia of Carp Virus to Suppress Antiviral Response in Zebrafish.Journal of virology · 2022Article
- Substitution of S179P in the Lyssavirus Phosphoprotein Impairs Its Interferon Antagonistic Function.Journal of virology · 2022Article
- Molecular Basis of Functional Effects of Phosphorylation of the C-Terminal Domain of the Rabies Virus P Protein.Journal of virology · 2022Article
- Deactivation of the antiviral state by rabies virus through targeting and accumulation of persistently phosphorylated STAT1.PLoS pathogens · 2022Article
- 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
- Antagonism of STAT3 signalling by Ebola virus.PLoS pathogens · 2021Article
- Phenotypic Divergence of P Proteins of Australian Bat Lyssavirus Lineages Circulating in Microbats and Flying Foxes.Viruses · 2021Article
- Street RABV Induces the Cholinergic Anti-inflammatory Pathway in Human Monocyte-Derived Macrophages by Binding to nAChr α7.Frontiers in immunology · 2021Article
- Early Transcriptional Changes in Rabies Virus-Infected Neurons and Their Impact on Neuronal Functions.Frontiers in microbiology · 2021Article
- The Dynamic Interface of Viruses with STATs.Journal of virology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many viruses target signal transducer and activator of transcription (STAT) 1 to antagonise antiviral interferon signalling, but targeting of STAT3, a pleiotropic molecule that mediates signalling by diverse cytokines, is poorly understood. Here, using lyssavirus infection, quantitative live cell imaging, innate immune signalling and protein interaction assays, and complementation/depletion of STAT expression, we show that STAT3 antagonism is conserved among P-proteins of diverse pathogenic lyssaviruses and correlates with pathogenesis. Importantly, P-protein targeting of STAT3 involves a highly selective mechanism whereby P-protein antagonises cytokine-activated STAT3-STAT1 heterodimers, but not STAT3 homodimers. RT-qPCR and reporter gene assays indicate that this results in specific modulation of interleukin-6-dependent pathways, effecting differential antagonism of target genes. These data provide novel insights into mechanisms by which viruses can modulate cellular function to support infection through discriminatory targeting of immune signalling complexes. The findings also highlight the potential application of selective interferon-antagonists as tools to delineate signalling by particular STAT complexes, significant not only to pathogen-host interactions but also cell physiology, development and cancer.
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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.