Department of Animal Science, Faculty of Agriculture, Bu-Ali Sina University, Hamedan, Iran
Abstract: (805 Views)
Extended Abstract
Background: Newcastle disease is one of the important diseases in the flock of chickens and roosters, which can result in many casualties. The disease is very dangerous and causes up to 90% death in the commercial flocks of broilers and laying hens in the case of an outbreak. This disease is caused by infection with malignant strains of Newcastle paramyxovirus. In addition to affecting chicken flocks and roosters, this contagious disease can spread to other poultry, such as turkeys, ducks, geese, quails, pheasants, and pigeons, and even ornamental birds, such as parrots. Fortunately, this disease has a vaccine, and if the necessary vaccines are injected into the herd at the appointed time, it will prevent its spread to the herd. The JS5-05 virus strain is one of the reference viruses that cause Newcastle disease, and other virus strains are compared with this strain in terms of pathogenicity and other characteristics. Previous reports suggest that immune responses to Newcastle disease have a genetic origin. Therefore, it can be expected that the expression of some genes will increase and the expression of others will decrease during the outbreak of this disease. These genes form a network in which they interact with each other. The gene network and protein-protein interaction in Newcastle disease caused by JS5-05 virus were investigated in the present study.
Methods: Gene expression data related to spleen cells of broiler chickens infected with the JS5-05 virus (patient treatment, three samples) and healthy broiler chickens (control treatment, three samples) were extracted from the NCBI website and the GEO Expression Omnibus database with the accession number GSE40100. Quality control and data normalization, as well as determining genes with different expressions, between the control and patient treatments at the level of p < 0.05 p-value and LogFC statistic (-2 < LogFC > +2), were done with GEO2R online software. The STRING resource was used to obtain the gene network. The network analyzer algorithm, which is a program loaded in CYTOSCAPE software, was used for network analysis. Three parameters were used to identify key genes in the network: the degree of centrality, betweenness centrality, and closeness centrality. These network topology measures were calculated using the CytoNCA plugin. Finally, DAVID online software was used to investigate the relationship between the central genes identified in the interactive network and Newcastle infection.
Results: In total, 4,720 out of 33,815 studied genes showed different expressions, of which significant differences were observed in the expression of 414 genes (p < 0.05 and -2 < LogFC > +2). These genes were located in an interactive network where each gene interacted with other genes. The 10 most important genes, including IFIH1, MX1, RSAD2, IFIT5, EIF2AK2, OASL, USP41, DHX58, CMPK2, and IFI6, formed the central core of the network, which involved various biological processes, including stopping the translation of the virus genome, stimulating the production of interferons and macrophages and stimulating the activity of some enzymes during Newcastle infection. The most important gene in the central network was the IFIH1 gene, which encodes a cell cycle protein called MAD5, an intracellular sensor for viral RNA that stimulates the innate immune response by stimulating the production of interferons. The results of the analysis of signaling pathways showed that the genes identified in this study were not only involved in Newcastle virus infection but were also active in other pathways, including infection with influenza A virus and herpes virus, as well as pathways that were active in the immune system.
Conclusion: All the genes in the central core of the gene network involved in response to the Newcastle virus had relationships with immune processes and defense responses to Newcastle infection, and therefore, a change was expected in their expressions during virus infection. Since there are different genotypes for these genes, it is suggested to examine the level of resistance to Newcastle disease in different genotypic groups for each gene and select the birds that have the superior genotype for the genes present in the central network to increase genetic resistance to Newcastle.
Background: Newcastle disease is one of the important diseases in the flock of chickens and roosters, which can result in many casualties. The disease is very dangerous and causes up to 90% death in the commercial flocks of broilers and laying hens in the case of an outbreak. This disease is caused by infection with malignant strains of Newcastle paramyxovirus. In addition to affecting chicken flocks and roosters, this contagious disease can spread to other poultry, such as turkeys, ducks, geese, quails, pheasants, and pigeons, and even ornamental birds, such as parrots. Fortunately, this disease has a vaccine, and if the necessary vaccines are injected into the herd at the appointed time, it will prevent its spread to the herd. The JS5-05 virus strain is one of the reference viruses that cause Newcastle disease, and other virus strains are compared with this strain in terms of pathogenicity and other characteristics. Previous reports suggest that immune responses to Newcastle disease have a genetic origin. Therefore, it can be expected that the expression of some genes will increase and the expression of others will decrease during the outbreak of this disease. These genes form a network in which they interact with each other. The gene network and protein-protein interaction in Newcastle disease caused by JS5-05 virus were investigated in the present study.
Methods: Gene expression data related to spleen cells of broiler chickens infected with the JS5-05 virus (patient treatment, three samples) and healthy broiler chickens (control treatment, three samples) were extracted from the NCBI website and the GEO Expression Omnibus database with the accession number GSE40100. Quality control and data normalization, as well as determining genes with different expressions, between the control and patient treatments at the level of p < 0.05 p-value and LogFC statistic (-2 < LogFC > +2), were done with GEO2R online software. The STRING resource was used to obtain the gene network. The network analyzer algorithm, which is a program loaded in CYTOSCAPE software, was used for network analysis. Three parameters were used to identify key genes in the network: the degree of centrality, betweenness centrality, and closeness centrality. These network topology measures were calculated using the CytoNCA plugin. Finally, DAVID online software was used to investigate the relationship between the central genes identified in the interactive network and Newcastle infection.
Results: In total, 4,720 out of 33,815 studied genes showed different expressions, of which significant differences were observed in the expression of 414 genes (p < 0.05 and -2 < LogFC > +2). These genes were located in an interactive network where each gene interacted with other genes. The 10 most important genes, including IFIH1, MX1, RSAD2, IFIT5, EIF2AK2, OASL, USP41, DHX58, CMPK2, and IFI6, formed the central core of the network, which involved various biological processes, including stopping the translation of the virus genome, stimulating the production of interferons and macrophages and stimulating the activity of some enzymes during Newcastle infection. The most important gene in the central network was the IFIH1 gene, which encodes a cell cycle protein called MAD5, an intracellular sensor for viral RNA that stimulates the innate immune response by stimulating the production of interferons. The results of the analysis of signaling pathways showed that the genes identified in this study were not only involved in Newcastle virus infection but were also active in other pathways, including infection with influenza A virus and herpes virus, as well as pathways that were active in the immune system.
Conclusion: All the genes in the central core of the gene network involved in response to the Newcastle virus had relationships with immune processes and defense responses to Newcastle infection, and therefore, a change was expected in their expressions during virus infection. Since there are different genotypes for these genes, it is suggested to examine the level of resistance to Newcastle disease in different genotypic groups for each gene and select the birds that have the superior genotype for the genes present in the central network to increase genetic resistance to Newcastle.
Type of Study: Research |
Subject:
ژنتیک و اصلاح نژاد دام
Received: 2024/08/17 | Accepted: 2025/06/1
Received: 2024/08/17 | Accepted: 2025/06/1
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