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MicroRNAs (miRNAs), as post-transcriptional regulators, play important roles in the process of viral infection through inhibiting virus replication or modulating host immune response. However, the role of miRNAs in host response against infectious bursal disease virus (IBDV) infection is still unclear. In this study, we found that gga-miR-454 of the host was decreased in response to IBDV infection and that transfection of DF-1 cells with miR-454 inhibited IBDV replication via directly targeting the specific sequence of IBDV genomic segment B, while blockage of endogenous miR-454 by inhibitors enhanced virus replication. Furthermore, gga-miR-454 increased the expression of IFN-β by targeting Suppressors of Cytokine Signaling 6 (SOCS6), enhancing the antiviral response of host cells. These findings highlight a crucial role of gga-miR-454 in host defense against IBDV infection.
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http://dx.doi.org/10.1016/j.virusres.2018.05.015 | DOI Listing |
Vet Microbiol
October 2025
Department of Veterinary Preventive Medicine, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, PR China; Jiangxi Provincial Key Laboratory for Animal Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, PR Chin
Cylindromatosis (CYLD), a deubiquitinase (DUB), removes K63-linked ubiquitin chains from idiosyncratic zymolytes, negatively regulating multifarious signaling channels, including NF-κ B, which is implicated in various cancers. Recently, the role of CYLD in antiviral immunity has gained attention, but its involvement in infectious Bursal diseases virus (IBDV) infection remains unclear. By coimmunoprecipitation combined with mass spectrometry analysis, we identified CYLD as a DUB bound to IBDV VP1.
View Article and Find Full Text PDFAvian Pathol
August 2025
U.S. Department of Agriculture, Agricultural Research Service, United States National Poultry Research Center, Southeast Poultry Research Laboratory, 934 College Station Road, Athens, Georgia, 30605, USA.
Seven lines of major histocompatibility complex (MHC)-B congenic specific pathogen free (SPF) chickens and two lines of non-B congenic SPF chickens with similar B haplotype but differing non-MHC genes were utilized to investigate the effect of the B locus on infectious bursal disease (IBD) development. In initial experiments, chickens were challenged at 28 days of age with the variant infectious bursal disease virus (IBDV) strain AL-2, classical IBDV strain STC, or very virulent (vv) IBDV strain rA. IBD severity was evaluated throughout the seven-day course of infection by assessing survivability and histopathological analysis of bursal lesion scores.
View Article and Find Full Text PDFBMC Genomics
August 2025
College of Animal Science and Technology, Yangzhou University, 48 East Wenhui Road, Yangzhou, 225009, Jiangsu, China.
Unlabelled: Infectious bursal disease virus (IBDV) causes a highly contagious and immunosuppressive disease that severely impacts the poultry industry. However, the molecular basis of IBDV-induced immunosuppression remains poorly understood. In this study, we investigate key genes implicated in this process, focusing on the interplay between metabolism and immune regulation.
View Article and Find Full Text PDFAvian Pathol
August 2025
Immunology Section, ICAR-Indian Veterinary Research Institute, Izatnagar-243122, India.
In the present study, antigen-chitosan-PLGA nanoparticles have been explored as the delivery system for inactivated whole IBD viral antigens. The immunized birds showed the peak antibody level (ELISA titer 4095.65±55.
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August 2025
Department of Poultry and Fish Diseases, Faculty of Veterinary Medicine, Alexandria University, Alexandria, 21944, Egypt.
Infectious bursal disease (IBD) is an immunosuppressive disease that increases susceptibility to avian coccidiosis, but the contrary is unclear. This study assessed whether the pathogenicity of the very virulent IBD virus was enhanced by previous (ET) infection of Egyptian Baladi chickens in a battery trial. Birds grouped as follows: G1 (control), G2 (ET, 1.
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