Base de dados : MEDLINE
Pesquisa : B04.613.807.070.100 [Categoria DeCS]
Referências encontradas : 2390 [refinar]
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[PMID]:29198037
[Au] Autor:Hu X; Chen S; Jia C; Xue S; Dou C; Dai Z; Xu H; Sun Z; Geng T; Cui H
[Ad] Endereço:Institute of Epigenetics and Epigenomics, College of Animal Science and Technology, Yangzhou University, 48 East Wenhui Road, Yangzhou, 225009, Jiangsu, China.
[Ti] Título:Gene expression profile and long non-coding RNA analysis, using RNA-Seq, in chicken embryonic fibroblast cells infected by avian leukosis virus J.
[So] Source:Arch Virol;163(3):639-647, 2018 Mar.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Avian leukosis virus J (ALVJ) infection induces hematopoietic malignancy in myeloid leukemia and hemangioma in chickens. However, little is known about the mechanisms underpinning the unique pathogenesis of ALVJ. In this study, we investigated the gene expression profiles of ALVJ-infected chicken cells and performed a comprehensive analysis of the long non-coding RNAs (lncRNAs) in CEF cells using RNA-Seq. As a result, 36 differentially expressed lncRNAs and 91 genes (FC > 2 and q-values < 0.05) were identified. Bioinformatics analysis revealed that these differentially expressed genes are involved in the innate immune response. Target prediction analysis revealed that these lncRNAs may act in cis or trans and affect the expression of genes which are involved in the anti-viral innate immune responses. Toll-like receptor, RIG-I receptor, NOD-like receptor and JAK-STAT signaling pathways were enriched. Notably, the induced expression of innate immunity genes, including B2M, DHX58, IFI27L2, IFIH1, IRF10, ISG12(2), MX, OAS*A, RSAD2, STAT1, TLR3, IL4I1, and IRF1 (FC > 2 and correlation > 0.95), were highly correlated with the upregulation of several lncRNAs, including MG066618, MG066617, MG066601, MG066629, MG066609 and MG066616. These findings identify the expression profile of lncRNAs in chicken CEF cells infected by ALVJ virus and provide new insights into the molecular mechanisms of ALVJ infection.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/genética
Fibroblastos/virologia
Interações Hospedeiro-Patógeno
RNA Longo não Codificante/genética
Transcriptoma/imunologia
[Mh] Termos MeSH secundário: Animais
Vírus da Leucose Aviária/crescimento & desenvolvimento
Vírus da Leucose Aviária/imunologia
Linhagem Celular
Embrião de Galinha
Biologia Computacional
Proteína DEAD-box 58/genética
Proteína DEAD-box 58/imunologia
Fibroblastos/imunologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Imunidade Inata
Janus Quinase 1/genética
Janus Quinase 1/imunologia
Proteínas NLR/genética
Proteínas NLR/imunologia
RNA Longo não Codificante/imunologia
Fatores de Transcrição STAT/genética
Fatores de Transcrição STAT/imunologia
Análise de Sequência de RNA
Transdução de Sinais
Receptores Toll-Like/genética
Receptores Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NLR Proteins); 0 (RNA, Long Noncoding); 0 (STAT Transcription Factors); 0 (Toll-Like Receptors); EC 2.7.10.2 (Janus Kinase 1); EC 3.6.4.13 (DEAD Box Protein 58)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171204
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3659-8


  2 / 2390 MEDLINE  
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[PMID]:29054407
[Au] Autor:Wang Z; Hou X; Wang Y; Xu A; Cao W; Liao M; Zhang R; Tang J
[Ad] Endereço:College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China.
[Ti] Título:Ubiquitination of non-lysine residues in the retroviral integrase.
[So] Source:Biochem Biophys Res Commun;494(1-2):57-62, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retroviral integrase catalyzes the integration of retroviral genome into host chromosomal DNA, which is a prerequisite of effective viral replication and infection. The human immunodeficiency virus type 1 (HIV-1) integrase has previously been reported to be regulated by the ubiquitination, but the molecular characterization of integrase ubiquitination is still unclear. In this study, we analyzed the ubiquitination of avian leukosis virus (ALV) integrase in detail. The ubiquitination assay showed that, like HIV-1, ALV integrase could also be modified by ubiquitination when expressed in 293 T and DF-1 cells. Domain mapping analysis revealed that the ubiquitination of ALV integrase might mainly occurred in the catalytic core and the N-terminal zinc-binding domains. Both lysine and non-lysine residues within integrase of ALV and HIV-1 were responsible for the ubiquitin conjugation, and the N-terminal HHCC zinc-binding motif might play an important role in mediating integrase ubiquitination. Interestingly, mass spectrometry analysis identified the Thr10 and Cys37 residues in the HHCC zinc-binding motif as the ubiquitination sites, indicating that ubiquitin may be conjugated to ALV integrase through direct interaction with the non-lysine residues. These findings revealed the detailed features of retroviral integrase ubiquitination and found a novel mechanism of ubiquitination mediated by the non-lysine residues within the N-terminal zinc-binding domain of integrase.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/enzimologia
Integrase de HIV/química
Integrase de HIV/metabolismo
Integrases/química
Integrases/metabolismo
Proteínas dos Retroviridae/química
Proteínas dos Retroviridae/metabolismo
Retroviridae/enzimologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Animais
Vírus da Leucose Aviária/genética
Vírus da Leucose Aviária/fisiologia
Linhagem Celular
Galinhas
Células HEK293
Integrase de HIV/genética
HIV-1/enzimologia
HIV-1/genética
HIV-1/fisiologia
Seres Humanos
Integrases/genética
Lisina/química
Mutagênese Sítio-Dirigida
Retroviridae/genética
Retroviridae/fisiologia
Proteínas dos Retroviridae/genética
Ubiquitinação
Zinco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Retroviridae Proteins); 0 (p31 integrase protein, Human immunodeficiency virus 1); EC 2.7.7.- (HIV Integrase); EC 2.7.7.- (Integrases); J41CSQ7QDS (Zinc); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171022
[St] Status:MEDLINE


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[PMID]:28493975
[Au] Autor:Wang Y; Yin Y; Lan X; Ye F; Tian K; Zhao X; Yin H; Li D; Xu H; Liu Y; Zhu Q
[Ad] Endereço:Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu, China.
[Ti] Título:Molecular characterization, expression of chicken TBK1 gene and its effect on IRF3 signaling pathway.
[So] Source:PLoS One;12(5):e0177608, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TRAF family member-associated NF-κB activator (TANK)-binding kinase1 (TBK1) is a serine-threonine kinase at the crossroads of multiple interferon (IFN)-inducing signaling pathways in innate immunity. The importance of TBK1 in antiviral immunity is well established in mammal models, but in chicken, the molecular characterization and potential function of TBK1 remain unclear. In the present study, the open-reading frame (ORF) of chicken TBK1 (chTBK1) was cloned and characterized. The sequencing results revealed that the chTBK1 ORF consists of 2190 base pairs (bp) encoding a deduced protein of 729 amino acid residues. Multiple sequence alignment analysis demonstrated chTBK1 similarity to other birds and mammals, which indicates that it is evolutionarily conserved. Quantitative real-time PCR (qRT-PCR) results showed that chTBK1 was ubiquitously expressed in chicken tissues and expression was especially high in immune tissues. In addition, the expression of chTBK1 was significantly up-regulated by infection with avian leukosis virus subgroup J (ALV-J) both in vivo and in chicken embryo fibroblasts (CEFs) challenged with ALV-J or stimulated with poly I:C in vitro. Consistent with the activation of chTBK1, the interferon regulatory factor 3 (IRF3) and IFNß gene in CEFs were also up-regulated after challenge with ALV-J or polyI:C. In contrast, the expression of IRF3 and IFNß in CEFs was significantly reduced by siRNA targeting the chTBK1 gene compared with a negative control (NC) during ALV-J infection or polyI:C transfection. In conclusion, our results demonstrated that chTBK1 may be an important immunoregulator for IRF3 and IFNß induction in response to viral stimulation in chicken.
[Mh] Termos MeSH primário: Galinhas/genética
Fator Regulador 3 de Interferon/metabolismo
Proteínas Serina-Treonina Quinases/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Leucose Aviária/genética
Leucose Aviária/virologia
Vírus da Leucose Aviária/fisiologia
Sequência de Bases
Embrião de Galinha
Galinhas/virologia
Biologia Computacional
Fibroblastos/metabolismo
Perfilação da Expressão Gênica
Técnicas de Silenciamento de Genes
Fator Regulador 3 de Interferon/genética
Interferon beta/genética
Interferon beta/metabolismo
Filogenia
Proteínas Serina-Treonina Quinases/química
Proteínas Serina-Treonina Quinases/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Alinhamento de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Regulatory Factor-3); 0 (RNA, Messenger); 77238-31-4 (Interferon-beta); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177608


  4 / 2390 MEDLINE  
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[PMID]:28349354
[Au] Autor:Shao H; Wang L; Sang J; Li T; Liu Y; Wan Z; Qian K; Qin A; Ye J
[Ad] Endereço:Ministry of Education Key Laboratory for Avian Preventive Medicine, and Key Laboratory of Jiangsu Preventive Veterinary Medicine, Yangzhou University, 12 Wenhui East Rd, Yangzhou, 225009, Jiangsu, People's Republic of China.
[Ti] Título:Novel avian leukosis viruses from domestic chicken breeds in mainland China.
[So] Source:Arch Virol;162(7):2073-2076, 2017 Jul.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Two novel avian leukosis viruses (ALVs) were isolated from 1380 whole blood samples taken from domestic chicken breeds in China. The two ALVs were uniquely different from the env (Envelope) genes of ALV A-J and carried an LTR (long terminal repeat) cluster from ALV-E. Large scale sequence analysis further showed that these ALVs (with different env and LTRs) were recently endemic in domestic chicken breeds in both China and Japan. The emergence of these novel ALVs is challenging the current ALV eradication program, and as such novel ALVs should be monitored in a timely and careful manner to stop their transmission and further recombination in the future.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/classificação
Leucose Aviária/virologia
Doenças das Aves Domésticas/virologia
Sequências Repetidas Terminais
Proteínas do Envelope Viral/genética
[Mh] Termos MeSH secundário: Animais
Animais Domésticos/virologia
Vírus da Leucose Aviária/genética
Vírus da Leucose Aviária/isolamento & purificação
Galinhas/virologia
China
Filogenia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Envelope Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3344-y


  5 / 2390 MEDLINE  
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[PMID]:28194372
[Au] Autor:Li Z; Luo Q; Xu H; Zheng M; Abdalla BA; Feng M; Cai B; Zhang X; Nie Q; Zhang X
[Ad] Endereço:Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural UniversityGuangzhou, China; Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding and the Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agricultur
[Ti] Título:MiR-34b-5p Suppresses Melanoma Differentiation-Associated Gene 5 ( ) Signaling Pathway to Promote Avian Leukosis Virus Subgroup J (ALV-J)-Infected Cells Proliferaction and ALV-J Replication.
[So] Source:Front Cell Infect Microbiol;7:17, 2017.
[Is] ISSN:2235-2988
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that has a similar replication cycle to multiple viruses and therefore can be used as a model system for viral entry into host cells. However, there are few reports on the genes or microRNAs (miRNAs) that are responsible for the replication of ALV-J. Our previous miRNA and RNA sequencing data showed that the expression of miR-34b-5p was significantly upregulated in ALV-J-infected chicken spleens compared to non-infected chicken spleens, but melanoma differentiation-associated gene 5 ( ) had the opposite expression pattern. In this study, a dual-luciferase reporter assay showed that is a direct target of miR-34b-5p. , overexpression of miR-34b-5p accelerated the proliferation of ALV-J-infected cells by inducing the progression from G2 to S phase and it promoted cell migration. Ectopic expression of inhibited ALV-J-infected cell proliferation, the cell cycle and cell migration, and knockdown of promoted proliferation, the cell cycle and migration. In addition, during ALV-J infections, can detect virus invasion and it triggers the MDA5 signaling pathway. overexpression can activate the MDA5 signaling pathway, and thus it can inhibit the mRNA and protein expression of the ALV-J gene and it can suppress virion secretion. In contrast, in response to the knockdown of by small interfering RNA (siRNA) or an miR-34b-5p mimic, genes in the MDA5 signaling pathway were significantly downregulated ( < 0.05), but the mRNA and protein expression of ALV-J and the sample-to-positive ratio of virion in the supernatants were increased. This indicates that miR-34b-5p is able to trigger the MDA5 signaling pathway and affect ALV-J infections. Together, these results suggest that miR-34b-5p targets to accelerate the proliferation and migration of ALV-J-infected cells, and it promotes ALV-J replication, via the MDA5 signaling pathway.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/fisiologia
Proliferação Celular
Interações Hospedeiro-Patógeno
Helicase IFIH1 Induzida por Interferon/antagonistas & inibidores
MicroRNAs/metabolismo
Transdução de Sinais
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Movimento Celular
Galinhas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.3389/fcimb.2017.00017


  6 / 2390 MEDLINE  
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[PMID]:28122976
[Au] Autor:Winans S; Larue RC; Abraham CM; Shkriabai N; Skopp A; Winkler D; Kvaratskhelia M; Beemon KL
[Ad] Endereço:Department of Biology, Johns Hopkins University, Baltimore, Maryland, USA.
[Ti] Título:The FACT Complex Promotes Avian Leukosis Virus DNA Integration.
[So] Source:J Virol;91(7), 2017 Apr 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:All retroviruses need to integrate a DNA copy of their genome into the host chromatin. Cellular proteins regulating and targeting lentiviral and gammaretroviral integration in infected cells have been discovered, but the factors that mediate alpharetroviral avian leukosis virus (ALV) integration are unknown. In this study, we have identified the FACT protein complex, which consists of SSRP1 and Spt16, as a principal cellular binding partner of ALV integrase (IN). Biochemical experiments with purified recombinant proteins show that SSRP1 and Spt16 are able to individually bind ALV IN, but only the FACT complex effectively stimulates ALV integration activity Likewise, in infected cells, the FACT complex promotes ALV integration activity, with proviral integration frequency varying directly with cellular expression levels of the FACT complex. An increase in 2-long-terminal-repeat (2-LTR) circles in the depleted FACT complex cell line indicates that this complex regulates the ALV life cycle at the level of integration. This regulation is shown to be specific to ALV, as disruption of the FACT complex did not inhibit either lentiviral or gammaretroviral integration in infected cells. The majority of human gene therapy approaches utilize HIV-1- or murine leukemia virus (MLV)-based vectors, which preferentially integrate near genes and regulatory regions; thus, insertional mutagenesis is a substantial risk. In contrast, ALV integrates more randomly throughout the genome, which decreases the risks of deleterious integration. Understanding how ALV integration is regulated could facilitate the development of ALV-based vectors for use in human gene therapy. Here we show that the FACT complex directly binds and regulates ALV integration efficiency and in infected cells.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/genética
Proteínas de Ciclo Celular/fisiologia
DNA Viral/fisiologia
Proteínas de Ligação a DNA/fisiologia
Proteínas de Grupo de Alta Mobilidade/fisiologia
Fatores de Transcrição/fisiologia
Fatores de Elongação da Transcrição/fisiologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Vírus da Leucose Aviária/enzimologia
Embrião de Galinha
Sequência Conservada
Células HEK293
Seres Humanos
Integrases/fisiologia
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Integração Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (DNA, Viral); 0 (DNA-Binding Proteins); 0 (High Mobility Group Proteins); 0 (SSRP1 protein, human); 0 (SUPT16H protein, human); 0 (Transcription Factors); 0 (Transcriptional Elongation Factors); EC 2.7.7.- (Integrases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE


  7 / 2390 MEDLINE  
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[PMID]:28065818
[Au] Autor:Feng W; Zhou D; Meng W; Li G; Zhuang P; Pan Z; Wang G; Cheng Z
[Ad] Endereço:College of Veterinary Medicine, Shandong Agricultural University, Tai'an, China; Weifang Medical University, Weifang, China.
[Ti] Título:Growth retardation induced by avian leukosis virus subgroup J associated with down-regulated Wnt/ß-catenin pathway.
[So] Source:Microb Pathog;104:48-55, 2017 Mar.
[Is] ISSN:1096-1208
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, induces growth retardation and neoplasia in chickens, leading to enormous economic losses in poultry industry. Increasing evidences showed several signal pathways involved in ALV-J infection. However, what signaling pathway involved in growth retardation is largely unknown. To explore the possible signaling pathway, we tested the cell proliferation and associated miRNAs in ALV-J infected CEF cells by CCK-8 and Hiseq, respectively. The results showed that cell proliferation was significantly inhibited by ALV-J and three associated miRNAs were identified to target Wnt/ß-catenin pathway. To verify the Wnt/ß-catenin pathway involved in cell growth retardation, we analyzed the key molecules of Wnt pathway in ALV-J infected CEF cells. Our data demonstrated that protein expression of ß-catenin was decreased significantly post ALV-J infection compared with the normal (P < 0.05). The impact of this down-regulation caused low expression of known target genes (Axin2, CyclinD1, Tcf4 and Lef1). Further, to obtain in vivo evidence, we set up an ALV-J infection model. Post 7 weeks infection, ALV-J infected chickens showed significant growth retardation. Subsequent tests showed that the expression of ß-catenin, Tcf1, Tcf4, Lef1, Axin2 and CyclinD1 were down-regulated in muscles of growth retardation chickens. Taken together, all data demonstrated that chicken growth retardation caused by ALV-J associated with down-regulated Wnt/ß-catenin signaling pathway.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/fisiologia
Leucose Aviária/metabolismo
Leucose Aviária/virologia
Galinhas
Fenótipo
Via de Sinalização Wnt
[Mh] Termos MeSH secundário: Animais
Leucose Aviária/complicações
Leucose Aviária/genética
Vírus da Leucose Aviária/classificação
Linhagem Celular
Proliferação Celular
Análise por Conglomerados
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
MicroRNAs/genética
Fatores de Transcrição/metabolismo
beta Catenina/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (Transcription Factors); 0 (beta Catenin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


  8 / 2390 MEDLINE  
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[PMID]:27890652
[Au] Autor:Dai M; Feng M; Liao M; Cao W
[Ad] Endereço:College of Veterinary Medicine, South China Agricultural University, Guangzhou, 510642, People's Republic of China; National and Regional Joint Engineering Laboratory for Medicament of Zoonosis Prevention and Control, People's Republic of China; Key Laboratory of Veterinary Vaccine Innovation of the
[Ti] Título:Inhibition of ERK/MAPK suppresses avian leukosis virus subgroup A and B replication.
[So] Source:Microb Pathog;102:29-35, 2017 Jan.
[Is] ISSN:1096-1208
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We have previously shown that the extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathway contributes to subgroup J avian leukosis virus (ALV-J) replication and tumorigenicity. However, a role for ERK/MAPK signaling in ALV-A and ALV-B replication is unknown. In this study we successfully constructed and recovered a recombinant form of ALV-A strain GD13-1 which showed similarities in growth to the parental wild type virus in vitro. ALV subgroups J, A or B all triggered ERK2 activation in primary CEF cells. ERK/MAPK inhibition markedly suppressed ALV-A and ALV-B replication as shown by extremely low levels of viral transcription and virus protein production. This finding provides evidence that ERK/MAPK signaling responses play important roles in ALV replication and may represent novel drug targets for therapeutic intervention strategies.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/efeitos dos fármacos
Vírus da Leucose Aviária/fisiologia
Leucose Aviária/metabolismo
Leucose Aviária/virologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Cultivadas
Galinhas
Fibroblastos/metabolismo
Fibroblastos/virologia
Flavonoides
Ordem dos Genes
Vetores Genéticos/genética
Genoma Viral
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Flavonoids); 0 (Protein Kinase Inhibitors); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170406
[Lr] Data última revisão:
170406
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE


  9 / 2390 MEDLINE  
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[PMID]:27881654
[Au] Autor:Plachý J; Reinisová M; Kucerová D; Senigl F; Stepanets V; Hron T; Trejbalová K; Elleder D; Hejnar J
[Ad] Endereço:Department of Viral and Cellular Genetics, Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
[Ti] Título:Identification of New World Quails Susceptible to Infection with Avian Leukosis Virus Subgroup J.
[So] Source:J Virol;91(3), 2017 Feb 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The J subgroup of avian leukosis virus (ALV-J) infects domestic chickens, jungle fowl, and turkeys. This virus enters the host cell through a receptor encoded by the tvj locus and identified as Na /H exchanger 1. The resistance to avian leukosis virus subgroup J in a great majority of galliform species has been explained by deletions or substitutions of the critical tryptophan 38 in the first extracellular loop of Na /H exchanger 1. Because there are concerns of transspecies virus transmission, we studied natural polymorphisms and susceptibility/resistance in wild galliforms and found the presence of tryptophan 38 in four species of New World quails. The embryo fibroblasts of New World quails are susceptible to infection with avian leukosis virus subgroup J, and the cloned Na /H exchanger 1 confers susceptibility on the otherwise resistant host. New World quails are also susceptible to new avian leukosis virus subgroup J variants but resistant to subgroups A and B and weakly susceptible to subgroups C and D of avian sarcoma/leukosis virus due to obvious defects of the respective receptors. Our results suggest that the avian leukosis virus subgroup J could be transmitted to New World quails and establish a natural reservoir of circulating virus with a potential for further evolution. IMPORTANCE: Since its spread in broiler chickens in China and Southeast Asia in 2000, ALV-J remains a major enzootic challenge for the poultry industry. Although the virus diversifies rapidly in the poultry, its spillover and circulation in wild bird species has been prevented by the resistance of most species to ALV-J. It is, nevertheless, important to understand the evolution of the virus and its potential host range in wild birds. Because resistance to avian retroviruses is due particularly to receptor incompatibility, we studied Na /H exchanger 1, the receptor for ALV-J. In New World quails, we found a receptor compatible with virus entry, and we confirmed the susceptibilities of four New World quail species in vitro We propose that a prospective molecular epidemiology study be conducted to identify species with the potential to become reservoirs for ALV-J.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/fisiologia
Leucose Aviária/genética
Leucose Aviária/virologia
Suscetibilidade a Doenças
Codorniz
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Aminoácidos
Animais
Leucose Aviária/metabolismo
Vírus da Leucose Aviária/classificação
Células Cultivadas
Resistência à Doença/genética
Evolução Molecular
Expressão Gênica
Loci Gênicos
Especificidade de Hospedeiro
Interações Hospedeiro-Patógeno
Filogenia
Polimorfismo Genético
Domínios e Motivos de Interação entre Proteínas
Trocadores de Sódio-Hidrogênio/química
Trocadores de Sódio-Hidrogênio/genética
Trocadores de Sódio-Hidrogênio/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Sodium-Hydrogen Exchangers)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161125
[St] Status:MEDLINE


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[PMID]:27486255
[Au] Autor:Feng M; Dai M; Cao W; Tan Y; Li Z; Shi M; Zhang X
[Ad] Endereço:Department of Animal Genetics, Breeding and Reproduction, College of Animal Science, South China Agricultural University, Guangzhou 510642, Guangdong, China.
[Ti] Título:ALV-J strain SCAU-HN06 induces innate immune responses in chicken primary monocyte-derived macrophages.
[So] Source:Poult Sci;96(1):42-50, 2017 Jan 01.
[Is] ISSN:1525-3171
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Avian leucosis virus subgroup J (ALV-J) can cause lifelong infection and can escape from the host immune defenses in chickens. Since macrophages act as the important defense line against invading pathogens in host innate immunity, we investigated the function and innate immune responses of chicken primary monocyte-derived macrophages (MDM) after ALV-J infection in this study. Our results indicated that ALV-J was stably maintained in MDM cells but that the viral growth rate was significantly lower than that in DF-1 cells. We also found that ALV-J infection significantly increased nitric oxide (NO) production, but had no effect on MDM phagocytic capacity. Interestingly, infection with ALV-J rapidly promoted the expression levels of Myxovirus resistance 1 (Mx) (3 h, 6 h), ISG12 (6 h), and interleukin-1ß (IL-1ß) (3 h, 12 h) at an early infection stage, whereas it sharply decreased the expression of Mx (24 h, 36 h), ISG12 (36 h), and made little change on IL-1ß (24 h, 36 h) production at a late infection stage in MDM cells. Moreover, the protein levels of interferon-ß (IFN-ß) and interleukin-6 (IL-6) had sharply increased in infected MDM cells from 3 to 36 h post infection (hpi) of ALV-J. And, the protein level of interleukin-10 (IL-10) was dramatically decreased at 36 hpi in MDM cells infected with ALV-J. These results demonstrate that ALV-J can induce host innate immune responses and we hypothesize that macrophages play an important role in host innate immune attack and ALV-J immune escape.
[Mh] Termos MeSH primário: Vírus da Leucose Aviária/imunologia
Leucose Aviária/imunologia
Galinhas
Imunidade Inata
Doenças das Aves Domésticas/imunologia
[Mh] Termos MeSH secundário: Animais
Leucose Aviária/virologia
Proteínas Aviárias/genética
Proteínas Aviárias/metabolismo
Linhagem Celular
Citocinas/genética
Citocinas/metabolismo
Feminino
Regulação da Expressão Gênica/imunologia
Macrófagos/imunologia
Macrófagos/virologia
Masculino
Doenças das Aves Domésticas/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Avian Proteins); 0 (Cytokines)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170412
[Lr] Data última revisão:
170412
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE



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