ArticleViruses2022
Differential Modulation of Innate Antiviral Profiles in the Intestinal Lamina Propria Cells of Chickens Infected with Infectious Bursal Disease Viruses of Different Virulence.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- A new recombinant avian metapneumovirus vaccine candidate provides complete protection against the novel variant infectious bursal disease virus in chickens.Veterinary research · 2026Article
- Key role of TLR3 in type I IFN expression and apoptosis induction in IBDV-infected chicken fibroblast cells.Frontiers in cellular and infection microbiology · 2026Article
- Chicken caspase-3 promotes IBDV replication via the cleavage of IRF7.Frontiers in microbiology · 2026Article
- Multi-Strain Probiotic Regulates the Intestinal Mucosal Immunity and Enhances the Protection of Piglets Against Porcine Epidemic Diarrhea Virus Challenge.Microorganisms · 2025Article
- A novel reassortant strain of the infectious bursal disease virus (IBDV ASPVB) from Iraqi broiler farms: A first-time molecular and histopathological investigation revealing new insights.Journal of advanced veterinary and animal research · 2025Article
- Exploring Variability: Inflammation Mediator Levels across Tissues and Time in Poultry Experimentally Infected by the G1a and G6 Genogroups of Infectious Bursal Disease Virus (IBDV).Animals : an open access journal from MDPI · 2024Article
- The complete protections induced by the oil emulsion vaccines of the novel variant infectious bursal disease viruses against the homologous challenges indicating the important roles of both VP2 and VP1 in the antigenicity and pathogenicity of the virus.Frontiers in veterinary science · 2024Article
- Infectious bursal disease virus affecting interferon regulatory factor 7 signaling through VP3 protein to facilitate viral replication.Frontiers in cellular and infection microbiology · 2024Article
- RNA-seq reveals role of cell-cycle regulating genes in the pathogenicity of a field very virulent infectious bursal disease virus.Frontiers in veterinary science · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infectious bursal disease virus (IBDV) is one of the most important infectious diseases of poultry around the world. Gut-associated lymphoid tissues (GALT) are the first line of defense of the host against the infection. The purpose of this study was to investigate the role of innate immune antiviral signaling triggered by Toll-like receptor 3 (TLR3), as well as macrophage activation and cytokine response in the intestinal lamina propria (ILP) cells after the oral challenge of IBDV in relation to IBDV virulence and disease pathogenesis. The results showed that the expression levels of TLR3, IRF7, IFN-α/β and the corresponding downstream antiviral factors OAS, PKR and Mx were all upregulated in the SPF chicken ILP cells at 8 h post-infection (hpi) and 12 hpi. Similarly, macrophages were activated, with the initial macrophage M1 activation observed at 8 hpi, but then it rapidly shifted to a non-protective M2-type. Both Th1 (IFN-γ, TNF-α, IL-12) and Th2 (IL-4 and IL-10) types of cytokines were differentially upregulated during the early stage of infection; however, the Th1 cytokines exhibited stronger activation before 8 hpi compared to those of the Th2 cytokines. Interestingly, differential regulations of gene expression induced by different IBDV strains with different virulence were detected. The HLJ0504-like very virulent (vv) IBDV strain NN1172 induced stronger activation of TLR3-IFN-α/β pathway, macrophages and the Th1/2 cytokines' expression, compared to those induced by the attenuated strain B87 at 8 hpi and 12 hpi in the ILP cells. In conclusion, the innate antiviral response mediated by the TLR3-IRF7 pathway, macrophage activation and cytokine expression in the GALT cells at the early stage of IBDV infection was differentially modulated, and the HLJ0504-like vvIBDV strain triggered stronger activation than the attenuated vaccine strain, and that may play an important role in the progression of disease.
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