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Pesquisa : G05.308.385 [Categoria DeCS]
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[PMID]:29302027
[Au] Autor:Campbell M; Watanabe T; Nakano K; Davis RR; Lyu Y; Tepper CG; Durbin-Johnson B; Fujimuro M; Izumiya Y
[Ad] Endereço:Department of Dermatology, School of Medicine, University of California Davis (UC Davis), Sacramento, CA, 95817, USA.
[Ti] Título:KSHV episomes reveal dynamic chromatin loop formation with domain-specific gene regulation.
[So] Source:Nat Commun;9(1):49, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The three-dimensional structure of chromatin organized by genomic loops facilitates RNA polymerase II access to distal promoters. The Kaposi's sarcoma-associated herpesvirus (KSHV) lytic transcriptional program is initiated by a single viral transactivator, K-Rta. Here we report the KSHV genomic structure and its relationship with K-Rta recruitment sites using Capture Hi-C analyses. High-resolution 3D viral genomic maps identify a number of direct physical, long-range, and dynamic genomic interactions. Mutant KSHV chromosomes harboring point mutations in the K-Rta responsive elements (RE) significantly attenuate not only the directly proximate downstream gene, but also distal gene expression in a domain-specific manner. Genomic loops increase in the presence of K-Rta, while abrogation of K-Rta binding impairs the formation of inducible genomic loops, decreases the expression of genes networked through the looping, and diminishes KSHV replication. Our study demonstrates that genomic architectural dynamics plays an essential role in herpesvirus gene expression.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
Genoma Viral/genética
Herpesvirus Humano 8/genética
Plasmídeos/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Linhagem Celular Tumoral
Cercopithecus aethiops
Seres Humanos
Transativadores/genética
Células Vero
Proteínas Virais/genética
Latência Viral/genética
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Trans-Activators); 0 (Viral Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02089-9


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[PMID]:28456021
[Au] Autor:Lupey-Green LN; Moquin SA; Martin KA; McDevitt SM; Hulse M; Caruso LB; Pomerantz RT; Miranda JL; Tempera I
[Ad] Endereço:Fels Institute for Cancer Research & Molecular Biology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
[Ti] Título:PARP1 restricts Epstein Barr Virus lytic reactivation by binding the BZLF1 promoter.
[So] Source:Virology;507:220-230, 2017 07.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Epstein Barr virus (EBV) genome persists in infected host cells as a chromatinized episome and is subject to chromatin-mediated regulation. Binding of the host insulator protein CTCF to the EBV genome has an established role in maintaining viral latency type, and in other herpesviruses, loss of CTCF binding at specific regions correlates with viral reactivation. Here, we demonstrate that binding of PARP1, an important cofactor of CTCF, at the BZLF1 lytic switch promoter restricts EBV reactivation. Knockdown of PARP1 in the Akata-EBV cell line significantly increases viral copy number and lytic protein expression. Interestingly, CTCF knockdown has no effect on viral reactivation, and CTCF binding across the EBV genome is largely unchanged following reactivation. Moreover, EBV reactivation attenuates PARP activity, and Zta expression alone is sufficient to decrease PARP activity. Here we demonstrate a restrictive function of PARP1 in EBV lytic reactivation.
[Mh] Termos MeSH primário: Infecções por Vírus Epstein-Barr/enzimologia
Infecções por Vírus Epstein-Barr/virologia
Herpesvirus Humano 4/fisiologia
Poli(ADP-Ribose) Polimerase-1/metabolismo
Regiões Promotoras Genéticas
Transativadores/genética
Ativação Viral
[Mh] Termos MeSH secundário: Linhagem Celular
Infecções por Vírus Epstein-Barr/genética
Regulação Viral da Expressão Gênica
Herpesvirus Humano 4/genética
Interações Hospedeiro-Patógeno
Seres Humanos
Poli(ADP-Ribose) Polimerase-1/genética
Ligação Proteica
Transativadores/metabolismo
Latência Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (BZLF1 protein, Herpesvirus 4, Human); 0 (Trans-Activators); EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180304
[Lr] Data última revisão:
180304
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  3 / 14086 MEDLINE  
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[PMID]:28743463
[Au] Autor:Rivas-Aravena A; Muñoz P; Jorquera P; Diaz A; Reinoso C; González-Catrilelbún S; Sandino AM
[Ad] Endereço:Comisión Chilena de Energía Nuclear, Departamento de Aplicaciones Nucleares, Laboratorio de Radiobiología Celular y Molecular. Nueva Bilbao 12501, Las Condes, Santiago, Chile; Universidad San Sebastián, Facultad de Ciencias, Lota 2465, Providencia, Santiago, Chile. Electronic address: andrea.rivas@c
[Ti] Título:Study of RNA-A Initiation Translation of The Infectious Pancreatic Necrosis Virus.
[So] Source:Virus Res;240:121-129, 2017 08 15.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The infectious pancreatic necrosis virus (IPNV) is a salmonid pathogen that causes significant economic losses to the aquaculture industry. IPNV is a non-enveloped virus containing two uncapped and non-polyadenylated double strand RNA genomic segments, RNA-A and RNA-B. The viral protein Vpg is covalently attached to the 5' end of both segments. There is little knowledge about its viral cycle, particularly about the translation of the RNAs. Through experiments using mono and bicistronic reporters, in this work we show that the 120-nucleotide-long 5'-UTR of RNA-A contains an internal ribosome entry site (IRES) that functions efficiently both in vitro and in salmon cells. IRES activity is strongly dependent on temperature. Also, the IRES structure is confined to the 5'UTR and is not affected by the viral coding sequence. This is the first report of IRES activity in a fish virus and can give us tools to generate antivirals to attack the virus without affecting fish directly.
[Mh] Termos MeSH primário: Infecções por Birnaviridae/veterinária
Doenças dos Peixes/virologia
Vírus da Necrose Pancreática Infecciosa/genética
Biossíntese de Proteínas
RNA Viral/genética
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas
Animais
Infecções por Birnaviridae/virologia
Regulação Viral da Expressão Gênica
Vírus da Necrose Pancreática Infecciosa/química
Vírus da Necrose Pancreática Infecciosa/metabolismo
Sítios Internos de Entrada Ribossomal
Conformação de Ácido Nucleico
RNA Mensageiro/química
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Viral/química
RNA Viral/metabolismo
Ribossomos/genética
Ribossomos/metabolismo
Salmo salar
Proteínas Virais/genética
Proteínas Virais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (Internal Ribosome Entry Sites); 0 (RNA, Messenger); 0 (RNA, Viral); 0 (Viral Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE


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[PMID]:29302061
[Au] Autor:Noda T; Murakami S; Nakatsu S; Imai H; Muramoto Y; Shindo K; Sagara H; Kawaoka Y
[Ad] Endereço:Division of Virology, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan. t-noda@infront.kyoto-u.ac.jp.
[Ti] Título:Importance of the 1+7 configuration of ribonucleoprotein complexes for influenza A virus genome packaging.
[So] Source:Nat Commun;9(1):54, 2018 01 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The influenza A virus genome is composed of eight single-stranded negative-sense RNAs. Eight distinct viral RNA segments (vRNAs) are selectively packaged into progeny virions, with eight vRNAs in ribonucleoprotein complexes (RNPs) arranged in a specific "1+7" pattern, that is, one central RNP surrounded by seven RNPs. Here we report the genome packaging of an artificially generated seven-segment virus that lacks the hemagglutinin (HA) vRNA. Electron microscopy shows that, even in the presence of only seven vRNAs, the virions efficiently package eight RNPs arranged in the same "1+7" pattern as wild-type virions. Next-generation sequencing reveals that the virions specifically incorporate host-derived 18S and 28S ribosomal RNAs (rRNAs) seemingly as the eighth RNP in place of the HA vRNA. These findings highlight the importance of the assembly of eight RNPs into a specific "1+7" configuration for genome packaging in progeny virions and suggest a potential role for cellular RNAs in viral genome packaging.
[Mh] Termos MeSH primário: Genoma Viral
Vírus da Influenza A/genética
Ribonucleoproteínas/metabolismo
Montagem de Vírus
[Mh] Termos MeSH secundário: Regulação Viral da Expressão Gênica/fisiologia
Células HEK293
Seres Humanos
RNA Viral/genética
Ribonucleoproteínas/química
Ribonucleoproteínas/genética
Proteínas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Viral); 0 (Ribonucleoproteins); 0 (Viral Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02517-w


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[PMID]:28743741
[Au] Autor:Zhao Z; Tang KW; Muylaert I; Samuelsson T; Elias P
[Ad] Endereço:From the Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology, Sahlgrenska Academy, University of Gothenburg, Box 440, SE-405 30 Gothenburg, Sweden.
[Ti] Título:CDK9 and SPT5 proteins are specifically required for expression of herpes simplex virus 1 replication-dependent late genes.
[So] Source:J Biol Chem;292(37):15489-15500, 2017 09 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DNA replication greatly enhances expression of the herpes simplex virus 1 (HSV-1) γ2 late genes by still unknown mechanisms. Here, we demonstrate that 5,6-dichloro-1-ß-d-ribofuranosylbenzimidazole (DRB), an inhibitor of CDK9, suppresses expression of γ2 late genes with an IC of 5 µm, which is at least 10 times lower than the IC value required for inhibition of expression of early genes. The effect of DRB could not be explained by inhibition of DNA replication or loading of RNA polymerase II to late promoters and subsequent reduction of transcription. Instead, DRB reduces accumulation of γ2 late mRNA in the cytoplasm. In addition, we show that siRNA-mediated knockdown of the transcription factor SPT5, but not NELF-E, also gives rise to a specific inhibition of HSV-1 late gene expression. Finally, addition of DRB reduces co-immunoprecipitation of ICP27 using an anti-SPT5 antibody. Our results suggest that efficient expression of replication-dependent γ2 late genes is, at least in part, regulated by CDK9 dependent co- and/or post-transcriptional events involving SPT5 and ICP27.
[Mh] Termos MeSH primário: Proteínas Cromossômicas não Histona/metabolismo
Quinase 9 Dependente de Ciclina/metabolismo
Replicação do DNA
Regulação Viral da Expressão Gênica
Herpesvirus Humano 1/fisiologia
Proteínas Imediatamente Precoces/metabolismo
Fatores de Elongação da Transcrição/metabolismo
Replicação Viral
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Antivirais/farmacologia
Linhagem Celular
Imunoprecipitação da Cromatina
Proteínas Cromossômicas não Histona/antagonistas & inibidores
Proteínas Cromossômicas não Histona/química
Proteínas Cromossômicas não Histona/genética
Biologia Computacional
Quinase 9 Dependente de Ciclina/antagonistas & inibidores
Quinase 9 Dependente de Ciclina/genética
Replicação do DNA/efeitos dos fármacos
Diclororribofuranosilbenzimidazol/farmacologia
Regulação Viral da Expressão Gênica/efeitos dos fármacos
Herpesvirus Humano 1/efeitos dos fármacos
Herpesvirus Humano 1/crescimento & desenvolvimento
Seres Humanos
Proteínas Imediatamente Precoces/química
Proteínas Imediatamente Precoces/genética
Imunoprecipitação
Mutação
Inibidores da Síntese de Ácido Nucleico/farmacologia
Regiões Promotoras Genéticas/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Interferência de RNA
Fatores de Transcrição/antagonistas & inibidores
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Fatores de Elongação da Transcrição/antagonistas & inibidores
Fatores de Elongação da Transcrição/química
Fatores de Elongação da Transcrição/genética
Proteínas Virais/antagonistas & inibidores
Proteínas Virais/química
Proteínas Virais/genética
Proteínas Virais/metabolismo
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Chromosomal Proteins, Non-Histone); 0 (ICP27 protein, human herpesvirus 1); 0 (Immediate-Early Proteins); 0 (Nucleic Acid Synthesis Inhibitors); 0 (Protein Kinase Inhibitors); 0 (Transcription Factors); 0 (Transcriptional Elongation Factors); 0 (Viral Proteins); 0 (negative elongation factor); 138673-72-0 (SPT5 transcriptional elongation factor); 53-85-0 (Dichlororibofuranosylbenzimidazole); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.806000


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[PMID]:28468879
[Au] Autor:Foscaldi S; D'Antuono A; Noval MG; de Prat Gay G; Scolaro L; Lopez N
[Ad] Endereço:Centro de Virología Animal, Instituto de Ciencia y Tecnología Dr. Cesar Milstein, Consejo Nacional de Ciencia y Tecnología, Buenos Aires, Argentina.
[Ti] Título:Regulation of Tacaribe Mammarenavirus Translation: Positive 5' and Negative 3' Elements and Role of Key Cellular Factors.
[So] Source:J Virol;91(14), 2017 Jul 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mammarenaviruses are enveloped viruses with a bisegmented negative-stranded RNA genome that encodes the nucleocapsid protein (NP), the envelope glycoprotein precursor (GPC), the RNA polymerase (L), and a RING matrix protein (Z). Viral proteins are synthesized from subgenomic mRNAs bearing a capped 5' untranslated region (UTR) and lacking 3' poly(A) tail. We analyzed the translation strategy of Tacaribe virus (TCRV), a prototype of the New World mammarenaviruses. A virus-like transcript that carries a reporter gene in place of the NP open reading frame and transcripts bearing modified 5' and/or 3' UTR were evaluated in a cell-based translation assay. We found that the presence of the cap structure at the 5' end dramatically increases translation efficiency and that the viral 5' UTR comprises stimulatory signals while the 3' UTR,specifically the presence of a terminal C+G-rich sequence and/or a stem-loop structure, down-modulates translation. Additionally, translation was profoundly reduced in eukaryotic initiation factor (eIF) 4G-inactivated cells, whereas depletion of intracellular levels of eIF4E had less impact on virus-like mRNA translation than on a cell-like transcript. Translation efficiency was independent of NP expression or TCRV infection. Our results indicate that TCRV mRNAs are translated using a cap-dependent mechanism, whose efficiency relies on the interplay between stimulatory signals in the 5' UTR and a negative modulatory element in the 3' UTR. The low dependence on eIF4E suggests that viral mRNAs may engage yet-unknown noncanonical host factors for a cap-dependent initiation mechanism. Several members of the family cause serious hemorrhagic fevers in humans. In the present report, we describe the mechanism by which Tacaribe virus, a prototypic nonpathogenic New World mammarenavirus, regulates viral mRNA translation. Our results highlight the impact of untranslated sequences and key host translation factors on this process. We propose a model that explains how viral mRNAs outcompete cellular mRNAs for the translation machinery. A better understanding of the mechanism of translation regulation of this virus can provide the bases for the rational design of new antiviral tools directed to pathogenic arenaviruses.
[Mh] Termos MeSH primário: Regiões 3´ não Traduzidas/genética
Regiões 5´ não Traduzidas/genética
Arenavirus do Novo Mundo/genética
Regulação Viral da Expressão Gênica
Biossíntese de Proteínas
RNA Mensageiro/genética
Sequências Reguladoras de Ácido Ribonucleico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Fator de Iniciação 4E em Eucariotos/metabolismo
Fator de Iniciação 4G em Eucariotos/metabolismo
Interações Hospedeiro-Patógeno
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (5' Untranslated Regions); 0 (Eukaryotic Initiation Factor-4E); 0 (Eukaryotic Initiation Factor-4G); 0 (RNA, Messenger); 0 (Regulatory Sequences, Ribonucleic Acid)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  7 / 14086 MEDLINE  
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[PMID]:28448849
[Au] Autor:Songock WK; Scott ML; Bodily JM
[Ad] Endereço:Department of Microbiology and Immunology, Center for Molecular and Tumor Virology, and Feist-Weiller Cancer Center, Louisiana State University Health Sciences Center, Shreveport, LA, USA.
[Ti] Título:Regulation of the human papillomavirus type 16 late promoter by transcriptional elongation.
[So] Source:Virology;507:179-191, 2017 07.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transcripts from the late promoter of human papillomavirus type 16 (HPV16) are upregulated upon host cell differentiation. Differentiation-dependent transcript regulation is thought to sequester viral antigens in the uppermost epithelial layers, facilitating immune evasion. The mechanisms regulating late promoter upregulation during differentiation are poorly characterized. We show that the late promoter is upregulated at the transcriptional level and that the viral enhancer stimulates promoter activity. Using kinase inhibition and chromatin immunoprecipitation analysis, we show evidence for differentiation-dependent enhancement of transcript elongation. Three factors that promote transcript elongation, cyclin dependent kinase 9 (CDK9), CDK8 (a subunit of the Mediator complex), and bromodomain containing protein 4 (Brd4) are recruited to viral genomes upon differentiation, and each plays a role in promoter activity. These results shed light on the transcriptional processes utilized by HPV16 for proper regulation of gene expression during the viral life cycle.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
Papillomavirus Humano 16/genética
Infecções por Papillomavirus/virologia
Regiões Promotoras Genéticas
Transcrição Genética
[Mh] Termos MeSH secundário: Quinase 8 Dependente de Ciclina/genética
Quinase 8 Dependente de Ciclina/metabolismo
Quinase 9 Dependente de Ciclina/genética
Quinase 9 Dependente de Ciclina/metabolismo
Papillomavirus Humano 16/metabolismo
Seres Humanos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Infecções por Papillomavirus/genética
Infecções por Papillomavirus/metabolismo
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BRD4 protein, human); 0 (Nuclear Proteins); 0 (Transcription Factors); EC 2.7.11.22 (Cyclin-Dependent Kinase 8); EC 2.7.11.22 (Cyclin-Dependent Kinase 9)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:27771562
[Au] Autor:Reed A; Lin L; Ostertag-Hill C; Wang Q; Wu Z; Miller-Morgan T; Jin L
[Ad] Endereço:Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, OR 97331, USA; Department of Microbiology, College of Science, Oregon State University, Corvallis, OR 97331, USA.
[Ti] Título:Detection of ORF6 protein associated with latent KHV infection.
[So] Source:Virology;500:82-90, 2017 01.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Koi herpesvirus (KHV) is highly pathogenic to Cyprinus carpio. KHV can also become latent in recovered fish and reactivate from latency under stressful conditions. Understanding KHV latency is important for development of strategies against herpesvirus latent infection. Our previous studies found KHV ORF6 mRNA is detectable during latent infection. In this study, ORF6 protein expression was investigated by a polyclonal antibody specific to ORF6 peptide. Positive staining by an immunofluorescence assay was observed in both KHV infected CCB (common carp brain) cells and IgM white blood cells (WBCs) from recovered KHV koi. Proteins at the expected size, 68kDa, and several different sizes can be detected during productive infection. Five potential sumoylation sites were identified in the ORF6 protein. Our study demonstrated that ORF6 protein is expressed in both productive infection and latent infection and may have different post-translational modifications during productive infection.
[Mh] Termos MeSH primário: Carpas/virologia
Doenças dos Peixes/virologia
Infecções por Herpesviridae/veterinária
Herpesviridae/fisiologia
Proteínas Virais/metabolismo
Latência Viral
[Mh] Termos MeSH secundário: Animais
Regulação Viral da Expressão Gênica
Herpesviridae/genética
Infecções por Herpesviridae/virologia
Processamento de Proteína Pós-Traducional
Proteínas Virais/genética
Ativação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171219
[Lr] Data última revisão:
171219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  9 / 14086 MEDLINE  
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[PMID]:28742148
[Au] Autor:Groussaud D; Khair M; Tollenaere AI; Waast L; Kuo MS; Mangeney M; Martella C; Fardini Y; Coste S; Souidi M; Benit L; Pique C; Issad T
[Ad] Endereço:INSERM, U1016, Institut Cochin, Paris, France.
[Ti] Título:Hijacking of the O-GlcNAcZYME complex by the HTLV-1 Tax oncoprotein facilitates viral transcription.
[So] Source:PLoS Pathog;13(7):e1006518, 2017 Jul.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The viral Tax oncoprotein plays a key role in both Human T-cell lymphotropic virus type 1 (HTLV-1)-replication and HTLV-1-associated pathologies, notably adult T-cell leukemia. Tax governs the transcription from the viral 5'LTR, enhancing thereby its own expression, via the recruitment of dimers of phosphorylated CREB to cAMP-response elements located within the U3 region (vCRE). In addition to phosphorylation, CREB is also the target of O-GlcNAcylation, another reversible post-translational modification involved in a wide range of diseases, including cancers. O-GlcNAcylation consists in the addition of O-linked-N-acetylglucosamine (O-GlcNAc) on Serine or Threonine residues, a process controlled by two enzymes: O-GlcNAc transferase (OGT), which transfers O-GlcNAc on proteins, and O-GlcNAcase (OGA), which removes it. In this study, we investigated the status of O-GlcNAcylation enzymes in HTLV-1-transformed T cells. We found that OGA mRNA and protein expression levels are increased in HTLV-1-transformed T cells as compared to control T cell lines while OGT expression is unchanged. However, higher OGA production coincides with a reduction in OGA specific activity, showing that HTLV-1-transformed T cells produce high level of a less active form of OGA. Introducing Tax into HEK-293T cells or Tax-negative HTLV-1-transformed TL-om1 T cells is sufficient to inhibit OGA activity and increase total O-GlcNAcylation, without any change in OGT activity. Furthermore, Tax interacts with the OGT/OGA complex and inhibits the activity of OGT-bound OGA. Pharmacological inhibition of OGA increases CREB O-GlcNAcylation as well as HTLV-1-LTR transactivation by Tax and CREB recruitment to the LTR. Moreover, overexpression of wild-type CREB but not a CREB protein mutated on a previously described O-GlcNAcylation site enhances Tax-mediated LTR transactivation. Finally, both OGT and OGA are recruited to the LTR. These findings reveal the interplay between Tax and the O-GlcNAcylation pathway and identify new key molecular actors involved in the assembly of the Tax-dependent transactivation complex.
[Mh] Termos MeSH primário: Produtos do Gene tax/metabolismo
Infecções por HTLV-I/virologia
Vírus 1 Linfotrópico T Humano/metabolismo
N-Acetilglucosaminiltransferases/metabolismo
Linfócitos T/virologia
beta-N-Acetil-Hexosaminidases/metabolismo
[Mh] Termos MeSH secundário: Acetilglucosamina/metabolismo
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/genética
Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo
Regulação Viral da Expressão Gênica
Produtos do Gene tax/genética
Infecções por HTLV-I/enzimologia
Infecções por HTLV-I/genética
Infecções por HTLV-I/metabolismo
Interações Hospedeiro-Patógeno
Vírus 1 Linfotrópico T Humano/genética
Seres Humanos
N-Acetilglucosaminiltransferases/genética
Processamento de Proteína Pós-Traducional
Linfócitos T/enzimologia
Linfócitos T/metabolismo
Transcrição Genética
beta-N-Acetil-Hexosaminidases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic AMP Response Element-Binding Protein); 0 (Gene Products, tax); 0 (tax protein, Human T-lymphotrophic virus 1); EC 2.4.1.- (N-Acetylglucosaminyltransferases); EC 2.4.1.- (O-GlcNAc transferase); EC 3.2.1.50 (hexosaminidase C); EC 3.2.1.52 (beta-N-Acetylhexosaminidases); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171213
[Lr] Data última revisão:
171213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006518


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[PMID]:29073268
[Au] Autor:Koyuncu OO; MacGibeny MA; Hogue IB; Enquist LW
[Ad] Endereço:Department of Molecular Biology, and Princeton Neuroscience Institute, Princeton University, Princeton, NJ, United States of America.
[Ti] Título:Compartmented neuronal cultures reveal two distinct mechanisms for alpha herpesvirus escape from genome silencing.
[So] Source:PLoS Pathog;13(10):e1006608, 2017 Oct.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alpha herpesvirus genomes encode the capacity to establish quiescent infections (i.e. latency) in the peripheral nervous system for the life of their hosts. Multiple times during latency, viral genomes can reactivate to start a productive infection, enabling spread of progeny virions to other hosts. Replication of alpha herpesviruses is well studied in cultured cells and many aspects of productive replication have been identified. However, many questions remain concerning how a productive or a quiescent infection is established. While infections in vivo often result in latency, infections of dissociated neuronal cultures in vitro result in a productive infection unless lytic viral replication is suppressed by DNA polymerase inhibitors or interferon. Using primary peripheral nervous system neurons cultured in modified Campenot tri-chambers, we previously reported that reactivateable, quiescent infections by pseudorabies virus (PRV) can be established in the absence of any inhibitor. Such infections were established in cell bodies only when physically isolated axons were infected at a very low multiplicity of infection (MOI). In this report, we developed a complementation assay in compartmented neuronal cultures to investigate host and viral factors in cell bodies that prevent establishment of quiescent infection and promote productive replication of axonally delivered genomes (i.e. escape from silencing). Stimulating protein kinase A (PKA) signaling pathways in isolated cell bodies, or superinfecting cell bodies with either UV-inactivated PRV or viral light particles (LP) promoted escape from genome silencing and prevented establishment of quiescent infection but with different molecular mechanisms. Activation of PKA in cell bodies triggers a slow escape from silencing in a cJun N-terminal kinase (JNK) dependent manner. However, escape from silencing is induced rapidly by infection with UVPRV or LP in a PKA- and JNK-independent manner. We suggest that viral tegument proteins delivered to cell bodies engage multiple signaling pathways that block silencing of viral genomes delivered by low MOI axonal infection.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica/genética
Inativação Gênica
Herpesvirus Humano 1/genética
Herpesvirus Suídeo 1/genética
Neurônios/virologia
Replicação Viral/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Genoma Viral/genética
Herpesvirus Humano 1/fisiologia
Suínos
Proteínas Virais/genética
Latência Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006608



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