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In the spring of 2023, 10 to 21-day-old chicks in a broiler duck farm in Shandong Province, China, developed swelling of the head and neck, moist eyes with mucous discharge, difficulty in walking, shrinking of the neck, and loose and disorganized coat. Anatomical observation revealed hemorrhages in the esophageal mucosa, myocardium, and liver, and severe hemorrhages in the trachea with copious inflammatory secretions. Soon after, similar symptoms appeared in a large number of ducks in the flock, which eventually led to the elimination of all the 20,000-odd newly introduced ducklings on the farm, resulting in huge economic losses. We detected duck plague virus in the tissues of liver, spleen and lungs of diseased and dead ducks, and successfully isolated the pathogenic strain, named SD423, by inoculating duck embryos and inoculating duck embryo fibroblasts. We successfully conducted animal regression experiments with the isolated strain, and the experimental animals in the 1 d of age group showed symptoms of swollen eyes and tearing, shrinking of the neck, crouching, and hemorrhage in organs such as the liver and intestines successively from the 3rd d. We sequenced the whole genome of the isolated duck plague strain, and by comparing the homology with the published duck plague virus whole sequences in Genbank, the virus strain obtained in this study had the highest homology with the Chinese virulent strain SD (MN518864.1), with nucleotide (nt) homology of about 99.90% and amino acid (aa) homology of about 99.75%, which indicated that the isolate is a virulent strain. Previously, it was reported that the natural infection of duck plague virus mainly occurs above 30 d of age, but the duck plague virus found in this study can naturally infect ducklings up to 20 d of age, and the mortality rate is as high as 100%. In this study, the pathogenicity test and whole genome sequence analysis of this isolate provided data support and theoretical basis for further research on pathogenicity and virulence-related gene analysis of duck plague virus.
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http://dx.doi.org/10.1016/j.psj.2024.103919 | DOI Listing |
Vet Microbiol
August 2025
Engineering Research Center of Southwest Animal Disease Prevention and Control Technology, Ministry of Education of the People's Republic of China, Chengdu 611130, China; International Joint Research Center for Animal Disease Prevention and Control of Sichuan Province, Chengdu 611130, China; Key Lab
Duck plague virus (DPV), an alphaherpesvirus causing severe economic losses in global waterfowl industries, adopts sophisticated strategies to subvert host antiviral immunity. Here, we identify DPV ICP27 as a pivotal immune evasion protein that concurrently inhibits both DNA (cGAS-STING) and RNA (RIG-I/MDA5-MAVS) innate immune sensing pathways-a novel function unreported in avian herpesviruses. Through co-transfection and infection assays in duck embryo fibroblasts (DEFs), we demonstrate that ICP27 suppresses key immune sensors' transcriptional and protein expression levels (STING, RIG-I) and the transcription factor IRF7.
View Article and Find Full Text PDFPoult Sci
August 2025
Institute of Veterinary Immunology and Green Drugs, Veterinary Department in College of Animal Science, State Key Laboratory of Green Pesticide, Guizhou University, Guiyang 550025, China. Electronic address:
Duck plague (DP), which is caused by duck plague virus (DPV), is an acute, highly contagious disease with an extremely high mortality rate, and poses a serious threat to the waterfowl industry. DPV, which is an immunosuppressive virus, can significantly suppress host innate immune responses during the late stages of infection. However, the specific mechanisms by which the DPV UL7 protein functions in the viral replication cycle and immune evasion remain unclear.
View Article and Find Full Text PDFPoult Sci
August 2025
Institute of Veterinary Immunology and Green Drugs, Veterinary Department in College of Animal Science, State Key Laboratory of Green Pesticide, Guizhou University, Guiyang 550025, China. Electronic address:
Interferon (IFN) critically regulates antiviral immunity, wherein its production level determines disease progression, many viruses disrupt these defenses through mechanisms that remain incompletely understood. This study investigates the effect of duck plague virus (DPV) infection on immune organs and elucidates the molecular mechanism by which its UL10 protein (pUL10) inhibits melanoma differentiation-associated protein 5 (MDA5)-mediated IFN-β production. DPV UL10 gene encodes pUL10, a virulence-associated protein critical for viral pathogenicity.
View Article and Find Full Text PDFVirulence
December 2025
Institute of Poultry Science, Shandong Academy of Agricultural Sciences/Shandong Provincial Key Laboratory of Livestock and Poultry Breeding, Jinan, China.
Duck enteritis virus (DEV) was identified as the etiological agent responsible for an outbreak of morbidity and mortality in adult ducks on a farm in Jiangsu, China. Diagnostic approaches confirmed that the outbreak was caused by the highly pathogenic DEV-JS2024 isolate. The clinical progression of the disease, characterized by lethargy, anorexia, ocular discharge, and high mortality, was accompanied by extensive hemorrhagic lesions in critical organs such as the liver, spleen, lungs, and bursa of Fabricius, consistent with known signs of DEV infection.
View Article and Find Full Text PDFVet Sci
May 2025
Engineering Research Center of Southwest Animal Disease Prevention and Control Technology, Ministry of Education of the People's Republic of China, Chengdu 611130, China.
Duck plague (DP), caused by duck plague virus (DPV), is a highly contagious and fatal disease among waterfowl. UL3.5, an unconserved gene belonging to the family, subfamily, and genus, is located downstream of UL3 and exhibits high variability in size and sequence, with an absence in herpes simplex virus (HSV).
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