Integrated host and viral transcriptome analyses reveal pathology and inflammatory response mechanisms to ALV-J injection in SPF chicken
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ABSTRACT:
PROVIDER: PRJEB15905 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1682080_1.fastq.gz | Fastqsanger.gz | |||
| ERR1682080_2.fastq.gz | Fastqsanger.gz | |||
| ERR1682081_1.fastq.gz | Fastqsanger.gz | |||
| ERR1682081_2.fastq.gz | Fastqsanger.gz | |||
| ERR1682082_1.fastq.gz | Fastqsanger.gz |
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Project description:Avian leukosis virus (ALV) causes substantial economic losses from mortality and decreased performance in poultry industry. To characterize the response to ALV challenge, we developed a novel methodology that combines four datasets: mRNA expression and their associated regulatory factors of miRNA and lncRNA, and ALV gene expression. Specific Pathogen-Free (SPF) layer chickens were assigned to the ALV-infected or control group. Spleen samples (n=6) were collected at 40 days post injection (dpi), and sequenced. Comparing the infected and non-infected groups, 864 genes, 7 miRNAs and 17 lncRNAs were differentially expressed.
2017-10-04 | E-MTAB-5135 | biostudies-arrayexpress
Project description:Avian leukosis virus (ALV) is detrimental to poultry health and causes substantial economic losses from mortality and decreased performance. Because tumorigenesis is a complex mechanism, the regulatory architecture of the immune system is likely to include the added dimensions of modulation by miRNAs and long-noncoding RNA (lncRNA). To characterize the response to ALV challenge, we developed a novel methodology that combines four datasets: mRNA expression and the associated regulatory factors of miRNA and lncRNA, and ALV gene expression. Specific Pathogen-Free (SPF) layer chickens were infected with ALV-J or maintained as non-injected controls. Spleen samples were collected at 40 days post injection (dpi), and sequenced. There were 864 genes, 7 miRNAs and 17 lncRNAs differentially expressed between infected and non-infected birds. The combined analysis of the 4 RNA expression datasets revealed that ALV infection is detected by pattern-recognition receptors (TLR9 and TLR3) leading to a type-I IFN mediated innate immune response that is modulated by IRF7 and IRF1. Co-expression network analysis of mRNA with miRNA, lncRNA and virus genes identified key elements within the complex networks utilized during ALV response. The integration of information from the host transcriptomic, epigenetic and virus response also has the potential to provide deeper insights into other host-pathogen interactions.
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Project description:We bed ALV-J-susceptible and ALV-J-resistant chickens. In this work, we find the different gene expression between ALV-J-susceptible and ALV-J-resistant chickens
2020-12-15 | GSE163135 | GEO
Project description:We bed ALV-J-susceptible and ALV-J-resistant chickens. In this work, we find the difference DNA methylation states between ALV-J-susceptible and ALV-J-resistant chickens
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Project description:Purpose: The goals of this study are to investigate the differentially expressed genes between ALV-J infected (WRR+) and uninfected (WRR-)chickens spleens by Illumina deep sequencing. Methods: 140-day-old female chickens of White Recessive Rock (WRR) were confirmed as J subgroup avian leukosis virus (ALV-J) infection. Total RNA from three ALV-J-infected spleens (designated: WRR1+, WRR2+, WRR3+) and three uninfected normal spleen samples (designated: WRR1-, WRR2-, WRR3-) was isolated by TRIzol following the manufacturer’s instruction (Invitrogen, CA, USA). RNA samples of three individuals within each group were pooled with equal amounts, and then were subjected to Illumina deep sequencing by Illumina Genome Analyzer IIx. Results: Through raw data processed, 49,979,648 and 43,704,401 clean reads with an average length of 101 bp, which represented total residues of 4,859,084,087 and 4,238,826,168 bp, were obtained for WRR- and WRR+ libraries, respectively. Subsequently, the clean reads in the two libraries were assembled. Altogether, 121,493 contigs were assembled with an average length of 927 bp (ranged from 300 bp to 23,402 bp), leading to generation of 82,829 unigenes. The length of unigenes varied from 351 bp to 28,928 bp, with an average length of 1,155 bp. Based on the FPKM value of each gene, 252 DEGs were identified by DEGseq package using Benjamini-q-value of 0.05 as a cut-off. In ALV-J infected spleens, 90 genes showed up-regulated and 162 showed down-regulated expression when compared to uninfected samples. Conclusions: Our study represents the first time to elucidate the ALV-J infected chickens’spleens at the transcription level by RNA-seq technology. A total of 252 genes were found to be differentially expressed in ALV-J infected spleens when compared to uninfected chickens. These genes can be considered as candidates for further study ALV-J invasion. Spleen mRNA profiles of 140-day-old ALV-J infected (WRR+) and uninfected (WRR-) female chickens of White Recessive Rock were generated by deep sequencing, using Illumina Genome Analyzer IIx.
2014-11-15 | E-GEOD-63226 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to investigate the differentially expressed genes between ALV-J infected (WRR+) and uninfected (WRR-)chickens spleens by Illumina deep sequencing. Methods: 140-day-old female chickens of White Recessive Rock (WRR) were confirmed as J subgroup avian leukosis virus (ALV-J) infection. Total RNA from three ALV-J-infected spleens (designated: WRR1+, WRR2+, WRR3+) and three uninfected normal spleen samples (designated: WRR1-, WRR2-, WRR3-) was isolated by TRIzol following the manufacturer’s instruction (Invitrogen, CA, USA). RNA samples of three individuals within each group were pooled with equal amounts, and then were subjected to Illumina deep sequencing by Illumina Genome Analyzer IIx. Results: Through raw data processed, 49,979,648 and 43,704,401 clean reads with an average length of 101 bp, which represented total residues of 4,859,084,087 and 4,238,826,168 bp, were obtained for WRR- and WRR+ libraries, respectively. Subsequently, the clean reads in the two libraries were assembled. Altogether, 121,493 contigs were assembled with an average length of 927 bp (ranged from 300 bp to 23,402 bp), leading to generation of 82,829 unigenes. The length of unigenes varied from 351 bp to 28,928 bp, with an average length of 1,155 bp. Based on the FPKM value of each gene, 252 DEGs were identified by DEGseq package using Benjamini-q-value of 0.05 as a cut-off. In ALV-J infected spleens, 90 genes showed up-regulated and 162 showed down-regulated expression when compared to uninfected samples. Conclusions: Our study represents the first time to elucidate the ALV-J infected chickens’spleens at the transcription level by RNA-seq technology. A total of 252 genes were found to be differentially expressed in ALV-J infected spleens when compared to uninfected chickens. These genes can be considered as candidates for further study ALV-J invasion.
2014-11-15 | GSE63226 | GEO
Project description:To elucidate the expression changes of host genes of SPF chickens infected with fowl adenovirus-4 at 48 hours post-infection. The hearts of SPF chickens infected with fowl adenovirus-4 were collected and high throughout sequenced. Compared with the control group, there were 1797 differentially expressed genes were obtained in the infection group, including 1082 up-regulated genes and 715 down-regulated genes.
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Project description:To survey avian leukosis virus subgroup J (ALV-J) integration in myeloid leukosis (ML) of chicken, we developed an ALV-J insertional identification platform based on hybrid-capture target enrichment and next-generation sequencing (NGS). In addition, we used gene expression profiling and bioinformatics to associate integration sites to transcriptional activity and to genetic features of the tumor cell genome. We selected six cases of ALV-J positive and diagnosed as ML for integration sites identify from commercial broiler breeder flocks in Guangdong Province of China between November 2011 and March 2012. All tumors were diagnosed on the basis of characteristic gross and microscopic lesions. Furthermore, PCR tests on the genomic DNA of tissues and virus isolation assay only showed ALV-J-specific positive results in previously study. We randomly chose 4 independent liver samples from the six cases for gene expression profile analysis. And 3 ALV-negative tissue samples from specific-pathogen-free (SPF) chickens at the same age were use as negative controls. Thus a total of 7 samples were hybridized, three representing control.
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Project description:Although research related to avian leukosis virus subgroup J (ALV-J) has lasted for more than a century, the systematic identification of host immune key factors against ALV-J infection has not been reported. In this study, we establish an infection model in which four-week-old SPF chickens are infected with ALV-J strain CHN06, after which the host immune response is detected. We found that the expression of two antiviral interferon-stimulated genes (ISGs) (Mx1 and IFIT5) were increased in ALV-J infected peripheral blood lymphocytes (PBL). A significant CD8+ T cell response induced by ALV-J appeared as early as seven days post-infection (DPI), and humoral immunity starting from 21 DPI differed greatly in the time scale of induction level. Meanwhile, the ALV-J viremia was significantly decreased before antibody production at 14 DPI, and eliminated at 21 DPI under a very low antibody level. The up-regulated CD8+ T cell in the thymus (14DPI) and PBL (7 DPI and 21 DPI) was detected, indicating that the thymus may provide the output of CD8+ T cell to PBL, which was related to virus clearance. Besides, up-regulated chemokine CXCLi1 at 7 DPI in PBL was observed, which may be related to the migration of the CD8+ T cell from the thymus to PBL. More importantly, the CD8 high+ T cell response of the CD8αβ phenotype may produce granzyme K, NK lysin, or IFN-γ for clearing viruses. These findings provide novel insights and direction for developing effective ALV-J vaccines.
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