ArticleVeterinary research2022
Duck plague virus UL41 protein inhibits RIG-I/MDA5-mediated duck IFN-β production via mRNA degradation activity.
Article in Veterinary research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Duck plague virus US2 promotes p62-mediated autophagic degradation of RIG-I to suppress antiviral signaling.Poultry science · 2026Article
- Alpha-herpesvirus UL55 synergizes with ICP27 to suppress type I interferon production through conserved and host-adapted mechanisms.Journal of virology · 2026Article
- Genomic Characterization of an Emergent Cross-Border Recombinant Duck Plague Virus With High Pathogenicity and Reduced Vaccine Efficacy in Guangxi, China.Transboundary and emerging diseases · 2026Article
- The neuro-immune crosstalk between periphery and central nervous system during acute immune response to virus-mimicking RNA in parrots.Royal Society open science · 2025Article
- PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- N-glycosylation of the envelope glycoprotein I is essential for the proliferation and virulence of the duck plague virus.Veterinary research · 2024Article
- Breaking Latent Infection: How ORF37/38-Deletion Mutants Offer New Hope against EHV-1 Neuropathogenicity.Viruses · 2024Article
- Pseudorabies virus VHS protein abrogates interferon responses by blocking NF-κB and IRF3 nuclear translocation.Virologica Sinica · 2024Article
- Mechanism of herpesvirus UL24 protein regulating viral immune escape and virulence.Frontiers in microbiology · 2023Review
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
Abstract
Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) are cytosolic pattern recognition receptors that initiate innate antiviral immunity. Recent reports found that duck RLRs significantly restrict duck plague virus (DPV) infection. However, the molecular mechanism by which DPV evades immune responses is unknown. In this study, we first found that the DPV UL41 protein inhibited duck interferon-β (IFN-β) production mediated by RIG-I and melanoma differentiation-associated gene 5 (MDA5) by broadly downregulating the mRNA levels of important adaptor molecules, such as RIG-I, MDA5, mitochondrial antiviral signalling protein (MAVS), stimulator of interferon gene (STING), TANK-binding kinase 1 (TBK1), and interferon regulatory factor (IRF) 7. The conserved sites of the UL41 protein, E229, D231, and D232, were responsible for this activity. Furthermore, the DPV CHv-BAC-ΔUL41 mutant virus induced more duck IFN-β and IFN-stimulated genes (Mx, OASL) production in duck embryo fibroblasts (DEFs) than DPV CHv-BAC parent virus. Our findings provide insights into the molecular mechanism underlying DPV immune evasion.
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