Innate immune genes up-regulated during infectious bursal disease virus infection in chicken embryos
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ABSTRACT:
PROVIDER: PRJNA555549 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9715900_1.fastq.gz | Fastqsanger.gz | |||
| SRR9715900_2.fastq.gz | Fastqsanger.gz | |||
| SRR9715910_1.fastq.gz | Fastqsanger.gz | |||
| SRR9715910_2.fastq.gz | Fastqsanger.gz | |||
| SRR9715901_1.fastq.gz | Fastqsanger.gz |
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Project description:Next generation sequencind applied to understanding bursal disease virus infection response in chicken embryos
2022-10-21 | GSE134542 | GEO
Project description:BACKGROUND:Infectious bursal disease is an acute immunosuppressive viral disease which significantly affect the economic in poultry industrial. Infectious bursal disease virus (IBDV) infection was known to destroy B lymphocytes, activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial Natural killer (IEL-NK) cells. RESULTS: The main objective of this study is to determine the innate immune response of chicken IEL-NK cells towards very virulent IBDV (vvIBDV) infection. Specific pathogen free (SPF) chickens were infected with vvIBDV for 0, 1 and 3 dpi. The IEL-NK cells were isolated and enriched from total IEL cells using the 28.4+ antibodies. The transcriptome sequencing was conducted in HiSeq2500 system and approximately 62 to 71 million paired-end reads generated per sample. The differential expression analysis was performed on the RNA-Seq data. On dpi 1, there are 838 genes up-regulated and 277 genes down-regulated. On dpi 3, there are 516 genes up-regulated whereas 750 genes down-regulated. According to pathway analysis, the differential expressed (DE) genes related to innate immune response are involved in several pathways such as cytokine-cytokine receptor, toll-like receptor and apoptosis pathway. CONCLUSION: The IEL-NK cells were de-activated after infected by vvIBDV through the down-regulation of several genes activate the NK cells such as IL18, TLR4 and TLR7/8. The IEL-NK cells were de-activated through up-regulation of expression for TGFB3 which inhibit the activation and function of NK cells by repressing the mTOR pathway. Meanwhile, the infection of vvIBDV induced apoptosis in IEL NK cells by increasing the expression level of some genes promote apoptosis such as CASP2, CASP8 and TLR3.
2020-05-28 | GSE123920 | GEO
Project description:Transcriptomics analysis reveals that severity of infectious bursal disease in White Leghorn inbred chicken lines is associated with greater bursal inflammation in vivo and more rapid induction of pro-inflammatory responses following ex vivo stimulation of primary bursal cells. In order to better understand differences in the outcome of infectious bursal disease virus (IBDV) infection, we inoculated very virulent (vv) IBDV into White Leghorn chickens from inbred line W that previously had over 24% mortality, and three inbred lines (15I, C.B4 and O) that previously had 0% mortality. Within each experimental group, some individuals experienced more severe disease than others but line 15I birds experienced milder disease based on average clinical scores, percentage of birds with gross pathology, average bursal lesion scores and average peak bursal virus titre. RNA-Seq analysis revealed that more severe disease was associated with a significant up-regulation of pathways involved in inflammation, cytoskeletal regulation by Rho GTPase, nicotinic acetylcholine receptor signaling, and Wnt signaling in the bursa. Primary bursal cells cultured from line W birds and stimulated ex vivo with LPS had a more rapid up-regulation of pro-inflammatory gene expression than cells from line 15I birds, and line W birds had a significantly greater percentage of KUL01+ macrophage cells in the BF than line 15I birds. We hypothesize that a more rapid induction of pro-inflammatory cytokine responses in line W birds causes excessive inflammation and clinical disease following IBDV infection compared to line 15I, and we suggest that pro-inflammatory pathways could be targeted to engineer more disease resistant birds in the future
2021-06-02 | GSE166026 | GEO
Project description:Infectious bursal disease virus (IBDV) is a highly contagious dsRNA virus (Birnaviridae) which causes immuno-suppression in chickens. Although largely controlled by vaccination, new, virulent strains of the virus mean that infectious bursal disease (IBD or ëGumboroí disease) still remains a threat to the poultry industry. The virus infects dividing IgM+ B-lymphocytes and the main site of viral replication is the bursa of Fabricius where B cells are produced. Infection is spread orally via contaminated feed and water. IBDV affects young birds, with the disease usually being diagnosed in 3-6 week old birds. Younger birds do not show clinical signs but are immuno-suppressed. Symptoms include anorexia, depression, diahorrea, ruffled feathers, immuno-suppression and bursal lesions. The disease peaks between 2-5 days post infection and is practically cleared by day 7. Mortality is variable but can be up to around 70% with very virulent strains of the disease. Even if birds survive, the resulting immuno-suppression and effect on egg production in layer birds is significant. Being able to breed commercial lines of birds for enhanced genetic resistance to IBDV is an obvious goal in the fight against the disease. Three-week-old chicks were inoculated with virus via an intra-nasal route and tissue samples were collected at 2, 3 and 4 days post-inoculation. Bursa and spleen tissues were examined from control and infected birds at 2, 3 and 4 days post-infection in birds known to be either susceptible or resistant to the virus. As well as understanding the host immune response to IBDV, we are interested in identifying genes involved in disease resistance and so we have analysed the gene expression profiles at these times, when the innate immune response is active. We assume that genes underlying resistance will be involved at this early stage of the host immune response.
2014-12-30 | E-TABM-1129 | biostudies-arrayexpress
Project description:Background: Avian infectious bursal disease virus (IBDV) is a major poultry disease which leads to significant losses of poultry industry. Dendritic cells (DCs), the only bridge communicated the innate and acquired immunity, have the most important antigen presenting ability and can significantly influence the pathogenicity of viruses. To understand the interaction between IBDV and DCs, microarray was used to analyze the response of DCs infected by IBDV. Results: Results showed that IBDV infection induced 479 up-regulated and 466 down-regulated mRNAs in chicken DCs. GO terms analysis suggested that transcription from RNA polymerase II promoter and RNA biosynthetic process were mainly enriched, whilst pathway analyses suggested that oxidative phosphorylation, T cell receptor and IL-17 signaling pathway might activated by IBDV infection. Moreover, we detected the microRNA (miRNA) and long non-coding RNA (lncRNA) alterations in IBDV-infected chicken DCs. Results identified 18 significant up- or down- regulated miRNAs and 441 significant up- or down-regulated lncRNAs in IBDV-stimulated DCs. Furthermore, we constructed 42 TF (transcription factors)-miRNA-mRNA interactions involving 1 TF, 3 miRNAs and 42 mRNAs in IBDV-stimulated DCs. Finally, we predicted the target genes of different expressed lncRNAs and constructed lncRNA-mRNA regulatory networks. Conclusions: Altogether, our research suggested a mechanism to explain how IBDV infection triggered an effective immune response in chicken DCs.
2016-03-24 | GSE79151 | GEO
Project description:Infectious bursal disease virus Genome sequencing and assembly
| PRJNA488138 | ENA
Project description:Infectious bursal disease is an acute immunosuppressive viral disease which significantly affect the economic in poultry industrial. Infectious bursal disease virus (IBDV) infection was known to destroy B lymphocytes, activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial Natural killer (IEL-NK) cells. The main objective of this study is to determine the innate immune response of chicken IEL-NK cells towards very virulent IBDV (vvIBDV) infection. Specific pathogen free (SPF) chickens were infected with vvIBDV for 0, 1 and 3 dpi. The IEL-NK cells were isolated and enriched from total IEL cells using the 28.4+ antibodies. The microRNA sequencing was conducted in MiSeq system and approximately 1.6 to 3.6 million single reads generated per sample. The differential expression analysis was performed on the miRNA-Seq data. there are 35 and 16 sRNAs were differentially expressed at 1 and 3 dpi, respectively. The SNORD101, gga-miR-222a and gga-miR-221-3p were up-regulated on Day 1 and 3 whereas gga-miR-30a-50, gga-miR-142-5p, gga-miR-32-5p and gga-miR-146b-5p were down-regulated on both days. gga-miR-217-5p and gga-miR-222b-5p with the highest fold change were involved in the regulation of tumor growth and apoptosis by targeting the MAPK signaling pathway. The vvIBDV replication was suppressed by overexpression of gga-miR-21 at 3 dpi. Some of the miRNAs were up-regulated with unknown reasons but the same findings were showed in other publications such as gga-miR-3538 and gga-miR-2954 which were up-regulated after being infected by other viruses, but the roles of these miRNA are not clear.
2022-12-31 | GSE148772 | GEO
Project description:Infectious bursal disease virus. Partial and complete genome sequencing for antigenic cartography
| PRJNA770494 | ENA
Project description:local strain P3009 segment B complete sequence of Infectious bursal disease virus
| PRJNA494626 | ENA
Project description:Viral diseases pose major threats to humans and other animals, including the billions of chickens that are an important food source as well as a public health concern due to zoonotic pathogens. Unlike humans and other typical mammals, the major histocompatibility complex (MHC) of chickens can confer decisive resistance or susceptibility to many viruses. Examples are Marek's disease virus (MDV) and Infectious bursal disease virus (IBDV). We used a new in vitro infection system and immunopeptidomics to identify peptides presented to T lymphocytes via classical MHC class II molecules.
2021-09-10 | PXD023954 | Pride