Transcriptional Profiling of Host Gene Expression in Chicken Embryo Fibroblasts Infected with Reticuloendotheliosis Virus Strain HA1101

Jiang, Miao; Bao, Yanqing; Ye, Jianqiang; Shao, Hongbo; Qian, Kun; Qin, Aijian

doi:10.1371/journal.pone.0126992

Cited by 19 publications

(11 citation statements)

References 67 publications

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“…Previously, we have identified miRNAs expression profile of bursa of Fabricius in SPF chickens in response to REV infections and discovered that miRNAs not only involved in the up-regulation of genes related to proapoptotic, proto-oncogene, and carcinogenic cytokines, but also involved in down-regulation of genes related to anti-apoptotic cytokines (Yu et al, 2017 ). By using microarray analysis, Ji Miao analyzed the transcripotme of CEF and found that genes involved in immune response played important roles in the pathogenicity of REV infection (Ji et al, 2015 ). Here we identified five significantly over-expressed oncogenes including HRAS, B-Raf, c-myc, c-fos, and c-jun.…”

Section: Discussionmentioning

confidence: 99%

Integrative Analyses of Transcriptome Sequencing Identify Functional miRNAs in the Chicken Embryo Fibroblasts Cells Infected With Reticuloendotheliosis Virus

Zhai

Gao

et al. 2018

Front. Genet.

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In this study, we found a much higher proportion of reticuloendotheliosis virus (REV) infected chicken embryo fibroblasts (CEF) were in active cell division phase than that of control cells which indicated that REV can affect the fate of CEF. So, we performed high-throughput sequencing and transcriptomic analysis to identify functional miRNAs, in order to figure out the possible mechanism in the interaction of REV with CEF. In total, 50 differentially expressed miRNAs (DEmiRNAs) were identified. Then target genes of DEmiRNAs were predicted and identified by transcriptome profile results. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment were conducted to analyze the identified target genes of miRNAs which showed that metabolism, cell cycle, and apoptosis were the most related pathways involved in infection of REV. We analyzed the genes related to cell cycle which indicated that CyclinD1-CDK6 complex played an important role in regulating the transition of the cell cycle from G1 phase to S phase during REV infection. Fluorescence microscope identification showed that REV inhibited the apoptosis of CEF which was in accordance with transcriptome results. A novel miRNA, named novel-72 was found, KEGG analysis was conducted to predict the biological function of its target genes which showed that those target genes were significantly enriched in mTOR signaling pathway and functioned to promote cell cycle and cell growth during the REV infection. In conclusion, REV could induce the up-regulation of cell metabolism, cell cycle and mTOR signaling pathway while inhibit apoptosis of the cell.

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Section: Discussionmentioning

confidence: 99%

Integrative Analyses of Transcriptome Sequencing Identify Functional miRNAs in the Chicken Embryo Fibroblasts Cells Infected With Reticuloendotheliosis Virus

Zhai

Gao

et al. 2018

Front. Genet.

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“…In chickens, immune organs such as thymuses, spleens, and bursas are the sites where T- and B-cells differentiate. REV is known to attack the reticuloendothelial cells or lymphocytes to induce humoral and cellular immune suppression, inducing the abnormal development of immune organs and finally inducing immunosuppression of the host ( 3 , 15 ). In the current study, REV infection caused atrophy of thymuses and bursas, indicating the impaired immune function.…”

Section: Discussionmentioning

confidence: 99%

Allicin Alleviates Reticuloendotheliosis Virus-Induced Immunosuppression via ERK/Mitogen-Activated Protein Kinase Pathway in Specific Pathogen-Free Chickens

et al. 2017

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Reticuloendotheliosis virus (REV), a gammaretrovirus in the Retroviridae family, causes an immunosuppressive, oncogenic, and runting–stunting syndrome in multiple avian hosts. Allicin, the main effective component of garlic, has a broad spectrum of pharmacological properties. The hypothesis that allicin could relieve REV-induced immune dysfunction was investigated in vivo and in vitro in the present study. The results showed that dietary allicin supplementation ameliorated REV-induced dysplasia and immune dysfunction in REV-infected chickens. Compared with the control groups, REV infection promoted the expression of inflammatory cytokines including interleukin (IL)-1β, IL-6, IL-10, interferon (IFN)-γ, and tumor necrosis factor-α (TNF-α), whereas, allicin reversed these changes induced by REV infection. The decreased levels of IFN-α, IFN-β, and IL-2 were observed in REV-infected chickens, which were significantly improved by allicin. Allicin suppressed the REV-induced high expression of toll-like receptors (TLRs) as well as melanoma differentiation-associated gene 5 (MDA5) and the activation of mitogen-activated protein kinase (MAPK) and the nuclear factor kappa B p65. REV stimulated the phosphorylation of JNK, ERK, and p38, the downstream key signaling molecules of MAPK pathway, while allicin retarded the augmented phosphorylation level induced by REV infection. The decreased phosphorylation level of ERK was associated with REV replication, suggesting that ERK signaling is involved in REV replication, and allicin can alleviate the REV-induced immune dysfunction by inhibiting the activation of ERK. In addition, REV infection induced oxidative damage in thymus and spleen, whereas allicin treatment significantly decreased the oxidative stress induced by REV infection, suggesting that the antioxidant effect of allicin should be at least partially responsible for the harmful effect of REV infection. In conclusion, the findings suggest that allicin alleviates the inflammation and oxidative damage caused by REV infection and exerts the potential anti-REV effect by blocking the ERK/MAPK pathway.

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“…In a recent study on chicken embryo fibroblast (CEF) cultures infected with reticuloendotheliosis virus HA1101 strain, differential expression of a number of genes leading to changes in several signalling pathways was reported [ 31 ]. We and others have shown upregulation of miR-155 in Rev-T-transformed cell lines and CEFs [ 32, 33 ].…”

Section: Introductionmentioning

confidence: 99%

Activation of gga-miR-155 by reticuloendotheliosis virus T strain and its contribution to transformation

Yao

Vasoya

Kgosana

et al. 2017

Journal of General Virology

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The v-rel oncoprotein encoded by reticuloendotheliosis virus T strain (Rev-T) is a member of the rel/NF-κB family of transcription factors capable of transformation of primary chicken spleen and bone marrow cells. Rapid transformation of avian haematopoietic cells by v-rel occurs through a process of deregulation of multiple protein-encoding genes through its direct effect on their promoters. More recently, upregulation of oncogenic miR-155 and its precursor pre-miR-155 was demonstrated in both Rev-T-infected chicken embryo fibroblast cultures and Rev-T-induced B-cell lymphomas. Through electrophoresis mobility shift assay and reporter analysis on the gga-miR-155 promoter, we showed that the v-rel-induced miR-155 overexpression occurred by the direct binding to one of the putative NF-κB binding sites. Using the v-rel-induced transformation model on chicken embryonic splenocyte cultures, we could demonstrate a dynamic increase in miR-155 levels during the transformation. Transcriptome profiles of lymphoid cells transformed by v-rel showed upregulation of miR-155 accompanied by downregulation of a number of putative miR-155 targets such as Pu.1 and CEBPβ. We also showed that v-rel could rescue the suppression of miR-155 expression observed in Marek’s disease virus (MDV)-transformed cell lines, where its functional viral homologue MDV-miR-M4 is overexpressed. Demonstration of gene expression changes affecting major molecular pathways, including organismal injury and cancer in avian macrophages transfected with synthetic mature miR-155, underlines its potential direct role in transformation. Our study suggests that v-rel-induced transformation involves a complex set of events mediated by the direct activation of NF-κB targets, together with inhibitory effects on microRNA targets.

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Transcriptional Profiling of Host Gene Expression in Chicken Embryo Fibroblasts Infected with Reticuloendotheliosis Virus Strain HA1101

Cited by 19 publications

References 67 publications

Integrative Analyses of Transcriptome Sequencing Identify Functional miRNAs in the Chicken Embryo Fibroblasts Cells Infected With Reticuloendotheliosis Virus

Integrative Analyses of Transcriptome Sequencing Identify Functional miRNAs in the Chicken Embryo Fibroblasts Cells Infected With Reticuloendotheliosis Virus

Allicin Alleviates Reticuloendotheliosis Virus-Induced Immunosuppression via ERK/Mitogen-Activated Protein Kinase Pathway in Specific Pathogen-Free Chickens

Activation of gga-miR-155 by reticuloendotheliosis virus T strain and its contribution to transformation

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