ArticleFrontiers in immunology2019
Isolation and Selection of Duck Primary Cells as Pathogenic and Innate Immunologic Cell Models for Duck Plague Virus.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Functional characterization ofThe veterinary quarterly · 2026Article
- ERAD inhibitor Eeyarestatin I (EerI) suppresses duck plague virus by restoring STING-mediated antiviral immunity.Poultry science · 2026Article
- Virulence attenuation of intestinal pathogenicity via combined gene deletion in duck enteritis vaccine strain restores gut microbiota balance and enhances safety.Poultry science · 2026Article
- Duck plague virus LORF2 utilizes RNF34 to inhibit antiviral innate immunity by ubiquitination and degradation of IRF7.PLoS pathogens · 2026Article
- In vivo inhibition of JAK-STAT signalling enhances high pathogenicity influenza virus replication in ducks.The Journal of general virology · 2026Article
- Metagenomic identification, isolation, and complete genome characterization of two novel picornaviruses in wild duck from Northeastern Siberia.Virology journal · 2025Article
- Mast cells-intestinal cancer cells crosstalk is mediated by TNF-alpha and sustained by the IL-33/ST2 axis.Cancer immunology, immunotherapy : CII · 2025Article
- Duck STING mediates antiviral autophagy directing the interferon signaling pathway to inhibit duck plague virus infection.Veterinary research · 2024Article
- Matrine and icariin can inhibit bovine viral diarrhoea virus replication by promoting type I interferon responseJournal of veterinary research · 2024Article
- Long non-coding RNA MM2P suppresses M1-polarized macrophages-mediated excessive inflammation to prevent sodium taurocholate-induced acute pancreatitis by blocking SHP2-mediated STAT3 dephosphorylation.Clinical and experimental medicine · 2023Article
- Duck plague virus UL41 protein inhibits RIG-I/MDA5-mediated duck IFN-β production via mRNA degradation activity.Veterinary research · 2022Article
- Avian Cell Culture Models to Study Immunomodulatory Properties of Bioactive Products.Animals : an open access journal from MDPI · 2022Review
- Duck Plague Virus Negatively Regulates IFN Signaling to Promote Virus ProliferationFrontiers in immunology · 2022Article
- Duck enteritis virus pUL47, as a late structural protein localized in the nucleus, mainly depends on residues 40 to 50 and 768 to 777 and inhibits IFN-β signalling by interacting with STAT1.Veterinary research · 2020Article
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21 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duck plague virus (DPV) is a representative pathogen transmitted among aquatic animals that causes gross lesions and immune inhibition in geese and ducks. The mechanism of organ tropism and innate immune evasion of DPV has not been completely deciphered due to a lack of cell models to study the innate immune manipulation and pathogenicity of aquatic viruses. In the present study, we isolated five types of duck primary cells [duck embryo fibroblasts (DEFs), neurons, astrocytes, peripheral blood mononuclear cells (PBMCs), and monocytes/macrophages] to identify appropriate cell models for DPV, using tropism infection and innate immunologic assays. Cells responded differently to stimulation with DNA viruses or RNA virus analogs. DPV infection exhibited broad tropism, as the recombinant virulent strain (CHv-GFP) infected DEFs, neurons, astrocytes, and monocytes/macrophages, but not the PBMCs, as the expression of EGFP was negligible. The basal levels of innate immunity molecules were highest in monocytes/macrophages and lower in DEFs and astrocytes. Conversely, the titer and genomic copy number of the attenuated virus strain was higher in DEFs and astrocytes than in neurons and monocytes/macrophages. The titer and genomic copy number of the attenuated virus strain were higher compared with the virulent strain in DEFs, neurons, and astrocytes. The innate immune response was not significantly induced by either DPV strain in DEFs, neurons, or astrocytes. The virulent strain persistently infected monocytes/macrophages, but the attenuated strain did so abortively, and this was accompanied by the phenomenon of innate immune inhibition and activation by the virulent and attenuated strains, respectively. Blockage of IFNAR signaling promoted replication of the attenuated strain. Pre-activation of IFNAR signaling inhibited infection by the virulent strain. The selection assay results indicated that induction of innate immunity plays an essential role in controlling DPV infection, and monocytes/macrophages are an important cell model for further investigations. Our study provided practical methods for isolating and culturing duck primary cells, and our results will facilitate further investigations of organ tropism, innate immune responses, latent infection, and the effectiveness of antiviral drugs for treating DPV and potentially other aerial bird pathogens.
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