ArticleFrontiers in cellular and infection microbiology2022
Nephropathogenic Infectious Bronchitis Virus Mediates Kidney Injury in Chickens
Article in Frontiers in cellular and infection microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Avian coronaviruses induce inflammatory responses by activating p38/MAPK signaling and NLRP3/caspase-1 inflammasomes through sphingosine-1-phosphate receptor 1.Veterinary research · 2026Article
- Coronavirus infectious bronchitis virus spike protein inhibits FUNDC1-mediated mitophagy to prevent nucleocapsid protein degradation.Journal of virology · 2026Article
- TRAF6, a gga-miR-7b Target, PromotesBiomolecules · 2026Article
- Multidimensional regulatory mechanisms of chicken immunity: focus on viral infection, intestinal microbiota and heat stress.Frontiers in veterinary science · 2026Review
- Avian coronavirus IBV-induced activation of the NLRP3-Caspase-1-IL-1β axis in renal collecting ducts contributes to nephropathogenesis.Journal of virology · 2025Article
- Nephropathogenic infectious bronchitis virus induces epithelial-mesenchymal transition of renal tubular epithelial cells through the TGF-β/p-P38 pathway causing uric acid excretion disorder in chickens.Journal of virology · 2025Article
- PEDV and BVDV coinfection activates the NF-κB pathway by a TLR7-dependent mechanism.Frontiers in microbiology · 2025Article
- Deciphering infected cell types, hub gene networks and cell-cell communication in infectious bronchitis virus via single-cell RNA sequencing.PLoS pathogens · 2024Article
- Emerging fatal gout disease in Chinese goslings linked to acute kidney injury induced by novel goose astrovirus infection.Frontiers in cellular and infection microbiology · 2024Article
- Key Aspects of Coronavirus Avian Infectious Bronchitis Virus.Pathogens (Basel, Switzerland) · 2023Review
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12 authors.
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Abstract
Nephropathogenic infectious bronchitis virus (NIBV) is one of the most important viral pathogens in the world poultry industry. Here, we used RT-qPCR, WB and immunofluorescence to explore the interaction between NIBV and the host innate immune system of the kidney. Multiple virions were found in the kidney tissues of the disease group under electron microscopy, and pathological changes such as structural damage of renal tubules and bleeding were observed by HE staining. In addition, we found that the mRNA levels of TLR7, TRAF6, and IKKβ were upregulated after NIBV infection. IRF7 mRNA levels decreased significantly at 5 dpi and increased significantly at 11 to 18 dpi. The NF-κB P65 mRNA level increased significantly at 5 to 18 dpi and decreased at 28 dpi. However, NIBV infection-induced NF-κB P65 protein levels were downregulated at multiple time points. Moreover, we demonstrated that the cytokine (IFN-γ, IL-8, and IL-6) mRNA and protein expression levels were increased significantly at multiple time points after NIBV infection. Furthermore, immunofluorescence analysis showed that NF-κB P65 and IFN-γ were mainly located in the nuclear or perinuclear region. The positive signal intensity of NF-κB P65 was significantly lower than that of the normal group at 1 to 5 dpi, and there was no significant change in the subsequent time period. The positive signal intensity of IFN-γ decreased significantly at 5 dpi, and increased significantly at 11 to 28 dpi. In conclusion, we found that NIBV promoted cytokine release through the TLR7/NF-κB signaling axis, thus causing kidney injury.
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