ArticleJournal of virology2019
Newcastle Disease Virus V Protein Degrades Mitochondrial Antiviral Signaling Protein To Inhibit Host Type I Interferon Production via E3 Ubiquitin Ligase RNF5.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- The multifaceted interactions between Newcastle disease virus proteins and host proteins: a systematic review.Virulence · 2024Pooled it
- Exploiting Ubiquitination: African Swine Fever Virus-Mediated Recruitment of Host E3 Ligases During Viral Infection and Immune Regulation.Pathogens (Basel, Switzerland) · 2026Review
- Article
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- Global evolution dynamics of genotype VI NDVs and dissection of the biological properties of strains from the prevalent sub-genotypes.Journal of virology · 2026Article
- DNAJA2 inhibits Newcastle disease virus replication by targeting its V protein to modulate the MDA5-MAVS pathway.BMC microbiology · 2025Article
- The intracellular virus-host interface of henipaviruses.Journal of virology · 2025Review
- Review of respiratory syndromes in poultry: pathogens, prevention, and control measures.Veterinary research · 2025Review
- Avian TRIM13 attenuates antiviral innate immunity by targeting MAVS for autophagic degradation.Autophagy · 2025Article
- Accessory viral protein, V, of Newcastle Disease Virus binds dsRNA to facilitate immune evasion.Virusdisease · 2025Article
- Equine lentivirus Gag protein degrades mitochondrial antiviral signaling protein via the E3 ubiquitin ligase Smurf1.Journal of virology · 2025Article
- Swine RNF5 positively regulates the antiviral activity of IFITM1 by mediating the degradation of ABHD16A.Journal of virology · 2025Article
- Recent advancements in the diverse roles of polymerase-associated proteins in the replication and pathogenesis of Newcastle disease virus.Veterinary research · 2025Review
- Novel Duck Orthoreovirus σA Protein Inhibits Interferon Signaling by Impeding STAT1/STAT2 Nuclear Translocation.Transboundary and emerging diseases · 2025Article
- Generation and characterization of chicken monocyte-derived dendritic cells.Frontiers in immunology · 2025Article
- RING finger protein 5 is a key anti-FMDV host factor through inhibition of virion assembly.PLoS pathogens · 2025Article
- Newcastle disease virus suppresses antigen presentation via inhibiting IL-12 expression in dendritic cells.Journal of Zhejiang University. Science. B · 2024Article
- Newcastle disease virus infection remodels plasma phospholipid metabolism in chickens.iScience · 2024Article
- The NP protein of Newcastle disease virus dictates its oncolytic activity by regulating viral mRNA translation efficiency.PLoS pathogens · 2024Article
- EFHD2 cooperates with E3 ubiquitin ligase Smurf1 to facilitate virus infection by promoting the degradation of TRAF6 in teleost fish.Journal of virology · 2024Article
4 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paramyxovirus establishes an intimate and complex interaction with the host cell to counteract the antiviral responses elicited by the cell. Of the various pattern recognition receptors in the host, the cytosolic RNA helicases interact with viral RNA to activate the mitochondrial antiviral signaling protein (MAVS) and subsequent cellular interferon (IFN) response. On the other hand, viruses explore multiple strategies to resist host immunity. In this study, we found that Newcastle disease virus (NDV) infection induced MAVS degradation. Further analysis showed that NDV V protein degraded MAVS through the ubiquitin-proteasome pathway to inhibit IFN-β production. Moreover, NDV V protein led to proteasomal degradation of MAVS through Lys362 and Lys461 ubiquitin to prevent IFN production. Further studies showed that NDV V protein recruited E3 ubiquitin ligase RNF5 to polyubiquitinate and degrade MAVS. Compared with levels for wild-type NDV infection, V-deficient NDV induced attenuated MAVS degradation and enhanced IFN-β production at the late stage of infection. Several other paramyxovirus V proteins showed activities of degrading MAVS and blocking IFN production similar to those of NDV V protein. The present study revealed a novel role of NDV V protein in targeting MAVS to inhibit cellular IFN production, which reinforces the fact that the virus orchestrates the cellular antiviral response to its own benefit.
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