ArticleViruses2019
The Nucleoprotein and Phosphoprotein of Peste des Petits Ruminants Virus Inhibit Interferons Signaling by Blocking the JAK-STAT Pathway.
Article in Viruses, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- African Swine Fever Virus pD345L Suppresses JAK-STAT Signaling by Selectively Triggering STAT1 Degradation.International journal of molecular sciences · 2026Article
- Ginsenoside Rh1 suppresses Peste des petits ruminants virus replication by inhibiting autophagy to promote interferon responses and restrict inflammatory responses.Frontiers in veterinary science · 2026Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Growth Arrest and DNA Damage Protein 45A Promotes PPRV Replication via the Downregulation of TBK1 Expression to Inhibit IFN-β Signaling Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Peste des petits ruminants virus (PPRV) induces ferroptosis via LONP1-mediated mitochondrial GPX4 degradation in cell culture.Journal of virology · 2025Article
- Structure, Attachment and Transmembrane Internalisation of Peste Des Petits Ruminants Virus.Veterinary medicine and science · 2025Review
- Plasminogen activator urokinase interacts with the fusion protein and antagonizes the growth of Peste des petits ruminants virus.Journal of virology · 2024Article
- Ribavirin inhibits peste des petits ruminants virus proliferationVeterinarni medicina · 2023Article
- ZebrafishJournal of virology · 2023Article
- Research Progress on Emerging Viral Pathogens of Small Ruminants in China during the Last Decade.Viruses · 2022Review
- Peste Des Petits Ruminants Virus N Protein Is a Critical Proinflammation Factor That Promotes MyD88 and NLRP3 Complex Assembly.Journal of virology · 2022Article
- Hemagglutinin protein of Peste des Petits Ruminants virus (PPRV) activates the innate immune response via Toll-like receptor 2 signaling.Virulence · 2021Article
- PPRV-induced novel miR-3 contributes to inhibit type I IFN production by targeting IRAK1.Journal of virology · 2021Article
- Caprine MAVS Is a RIG-I Interacting Type I Interferon Inducer Downregulated by Peste des Petits Ruminants Virus Infection.Viruses · 2021Article
- Antiviral Effectivity of Favipiravir Against Peste Des Petits Ruminants Virus Is Mediated by the JAK/STAT and PI3K/AKT Pathways.Frontiers in veterinary science · 2021Article
- Evasion of Host Antiviral Innate Immunity by Paramyxovirus Accessory Proteins.Frontiers in microbiology · 2021Review
- Inhibition of eIF2α Phosphorylation by Peste des Petits Ruminant Virus Phosphoprotein Facilitates Viral Replication.Frontiers in veterinary science · 2021Article
- MicroRNA-1 Negatively Regulates Peripheral NK Cell Function via Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) Signaling Pathways During PPRV Infection.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peste des petits ruminants virus (PPRV) is associated with global peste des petits ruminants resulting in severe economic loss. Peste des petits ruminants virus dampens host interferon-based signaling pathways through multiple mechanisms. Previous studies deciphered the role of V and C in abrogating IFN-β production. Moreover, V protein directly interacted with signal transducers and activators of transcription 1 (STAT1) and STAT2 resulting in the impairment of host IFN responses. In our present study, PPRV infection inhibited both IFN-β- and IFN-γ-induced activation of IFN-stimulated response element (ISRE) and IFN-γ-activated site (GAS) element, respectively. Both N and P proteins, functioning as novel IFN response antagonists, markedly suppressed IFN-β-induced ISRE and IFN-γ-induced GAS promoter activation to impair downstream upregulation of various interferon-stimulated genes (ISGs) and prevent STAT1 nuclear translocation. Specifically, P protein interacted with STAT1 and subsequently inhibited STAT1 phosphorylation, whereas N protein neither interacted with STAT1 nor inhibited STAT1 phosphorylation as well as dimerization, suggesting that the N and P protein antagonistic effects were different. Though they differed in their relationship to STAT1, both proteins blocked JAK-STAT signaling, severely negating the host antiviral immune response. Our study revealed a new mechanism employed by PPRV to evade host innate immune response, providing a platform to study the interaction of paramyxoviruses and host response.
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Registered trials
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