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  1 / 486 MEDLINE  
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[PMID]:28850829
[Au] Autor:Howard K; Cherezova L; DeMaster LK; Rose TM
[Ad] Endereço:Center for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, WA, USA; Department of Global Health, University of Washington, Seattle, WA, USA. Electronic address: kellie.howard@covance.com.
[Ti] Título:ORF73 LANA homologs of RRV and MneRV2 contain an extended RGG/RG-rich nuclear and nucleolar localization signal that interacts directly with importin ß1 for non-classical nuclear import.
[So] Source:Virology;511:152-164, 2017 Nov.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The latency-associated nuclear antigens (LANA) of KSHV and macaque RFHVMn, members of the RV1 rhadinovirus lineage, are closely related with conservation of complex nuclear localization signals (NLS) containing bipartite KR-rich motifs and RG-rich domains, which interact distinctly with importins α and ß1 for nuclear import via classical and non-classical pathways, respectively. RV1 LANAs are expressed in the nucleus of latently-infected cells where they inhibit replication and establish a dominant RV1 latency. Here we show that LANA homologs of macaque RRV and MneRV2 from the more distantly-related RV2 lineage, lack the KR-rich NLS, and instead have a large RG-rich NLS with multiple RG dipeptides and a conserved RGG motif. The RG-NLS interacts uniquely with importin ß1, which mediates nuclear import and accumulation of RV2 LANA in the nucleolus. The alternative nuclear import and localization of RV2 LANA homologs may contribute to the dominant RV2 lytic replication phenotype.
[Mh] Termos MeSH primário: Transporte Ativo do Núcleo Celular
Antígenos Nucleares/metabolismo
Interações Hospedeiro-Patógeno
Mapeamento de Interação de Proteínas
Rhadinovirus/fisiologia
Proteínas Virais/metabolismo
beta Carioferinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos Nucleares/genética
Macaca mulatta
Macaca nemestrina
Ligação Proteica
Sinais Direcionadores de Proteínas
Proteínas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Nuclear); 0 (Protein Sorting Signals); 0 (Viral Proteins); 0 (beta Karyopherins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE


  2 / 486 MEDLINE  
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[PMID]:28821622
[Au] Autor:Foreman HC; Armstrong J; Santana AL; Krug LT; Reich NC
[Ad] Endereço:From the Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York 11794.
[Ti] Título:The replication and transcription activator of murine gammaherpesvirus 68 cooperatively enhances cytokine-activated, STAT3-mediated gene expression.
[So] Source:J Biol Chem;292(39):16257-16266, 2017 Sep 29.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gammaherpesviruses (γHVs) have a dynamic strategy for lifelong persistence, involving productive infection, latency, and intermittent reactivation. In latency reservoirs, such as B lymphocytes, γHVs exist as viral episomes and express few viral genes. Although the ability of γHV to reactivate from latency and re-enter the lytic phase is challenging to investigate and control, it is known that the γHV replication and transcription activator (RTA) can promote lytic reactivation. In this study, we provide first evidence that RTA of murine γΗV68 (MHV68) selectively binds and enhances the activity of tyrosine-phosphorylated host STAT3. STAT3 is a transcription factor classically activated by specific tyrosine 705 phosphorylation (pTyr -STAT3) in response to cytokine stimulation. pTyr -STAT3 forms a dimer that avidly binds a consensus target site in the promoters of regulated genes, and our results indicate that RTA cooperatively enhances the ability of pTyr -STAT3 to induce expression of a STAT3-responsive reporter gene. As indicated by coimmunoprecipitation, in latently infected B cells that are stimulated to reactivate MHV68, RTA bound specifically to endogenous pTyr -STAT3. An binding assay confirmed that RTA selectively recognizes pTyr -STAT3 and indicated that the C-terminal transactivation domain of RTA was required for enhancing STAT3-directed gene expression. The cooperation of these transcription factors may influence both viral and host genes. During MHV68 infection, pTyr -STAT3 promoted the temporal expression of ORF59, a viral replication protein. Our results demonstrate that MHV68 RTA specifically recognizes and recruits activated pTyr -STAT3 during the lytic phase of infection.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Regulação da Expressão Gênica
Proteínas Imediatamente Precoces/metabolismo
Interleucina-6/metabolismo
Receptores de Interleucina-6/agonistas
Rhadinovirus/fisiologia
Fator de Transcrição STAT3/agonistas
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Linfócitos B/imunologia
Linfócitos B/virologia
Linhagem Celular
Dimerização
Genes Reporter
Seres Humanos
Proteínas Imediatamente Precoces/química
Proteínas Imediatamente Precoces/genética
Camundongos
Mutação
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Fosforilação
Domínios e Motivos de Interação entre Proteínas
Processamento de Proteína Pós-Traducional
Receptores de Interleucina-6/metabolismo
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Rhadinovirus/imunologia
Fator de Transcrição STAT3/química
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais
Transativadores/química
Transativadores/genética
Tirosina/metabolismo
Ativação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immediate-Early Proteins); 0 (Interleukin-6); 0 (Peptide Fragments); 0 (Receptors, Interleukin-6); 0 (Recombinant Fusion Proteins); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (Trans-Activators); 0 (gene 50 protein, gammaherpesvirus 68); 42HK56048U (Tyrosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.786970


  3 / 486 MEDLINE  
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[PMID]:28767707
[Au] Autor:Terrell S; Speck SH
[Ad] Endereço:Department of Microbiology & Immunology, Emory University School of Medicine, Atlanta, GA, United States of America.
[Ti] Título:Murine gammaherpesvirus M2 antigen modulates splenic B cell activation and terminal differentiation in vivo.
[So] Source:PLoS Pathog;13(8):e1006543, 2017 Aug.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Murine gammaherpesvirus 68 (MHV68) infection of laboratory strains of mice has provided a tractable small animal model for dissecting gammaherpesvirus pathogenesis. The MHV68 latency associated antigen M2 promotes viral latency establishment in germinal center (GC) B cells and plays an important role in virus infection of plasma cells (PCs), which is linked to virus reactivation. More recently, M2 has been highlighted as a potent immunomodulatory molecule capable of hindering both cell-mediated and humoral immunity to MHV68 infection and subsequent challenges. M2 expression in B cells results in activation of B cell receptor signaling pathways that promote proliferation, differentiation, and cytokine production-a hallmark of gammaherpesviruses. In this study, we utilized an adoptive transfer model to explore the biological consequence of M2 expression in activated B cells in vivo. Secondly, we engineered and validated two independent MHV68 M2 reporter viruses that track M2 protein expression in latently infected B cells during infection. Here we demonstrate that upon adoptive transfer into naive mice, M2 expression promotes activated primary B cells to competitively establish residency in the spleen as either a GC B cell or a PC, most notably in the absence of an ongoing GC reaction. Moreover, M2 antigen drives robust PC differentiation and IL10 production in vivo in the absence of other viral factors. Lastly, we confirm that M2 expression during MHV68 infection is localized to the GC compartment, which is a long term latency reservoir for gammaherpesviruses. Overall, these observations are consistent with, and extend upon previous reports of M2 function in B cells and within the context of MHV68 infection. Moreover, this work provides support for a model by which M2-driven dysregulation of B cell function compromises multiple aspects of antiviral immunity to achieve persistence within the infected host.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Linfócitos B/virologia
Infecções por Herpesviridae/imunologia
Ativação Linfocitária/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Diferenciação Celular/imunologia
Modelos Animais de Doenças
Citometria de Fluxo
Centro Germinativo/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Rhadinovirus/imunologia
Baço/imunologia
Proteínas Virais
Latência Viral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (M2 protein, murine gammaherpesvirus 68); 0 (Viral Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006543


  4 / 486 MEDLINE  
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[PMID]:28732227
[Au] Autor:Darrah EJ; Stoltz KP; Ledwith M; Tarakanova VL
[Ad] Endereço:Department of Microbiology and Immunology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, United States.
[Ti] Título:ATM supports gammaherpesvirus replication by attenuating type I interferon pathway.
[So] Source:Virology;510:137-146, 2017 Oct.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ataxia-Telangiectasia mutated (ATM) kinase participates in multiple networks, including DNA damage response, oxidative stress, and mitophagy. ATM also supports replication of diverse DNA and RNA viruses. Gammaherpesviruses are prevalent cancer-associated viruses that benefit from ATM expression during replication. This proviral role of ATM had been ascribed to its signaling within the DNA damage response network; other functions of ATM have not been considered. In this study increased type I interferon (IFN) responses were observed in ATM deficient gammaherpesvirus-infected macrophages. Using a mouse model that combines ATM and type I IFN receptor deficiencies we show that increased type I IFN response in the absence of ATM fully accounts for the proviral role of ATM during gammaherpesvirus replication. Further, increased type I IFN response rendered ATM deficient macrophages more susceptible to antiviral effects of type II IFN. This study identifies attenuation of type I IFN responses as the primary mechanism underlying proviral function of ATM during gammaherpesvirus infection.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno
Interferon Tipo I/antagonistas & inibidores
Rhadinovirus/fisiologia
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Proteínas Mutadas de Ataxia Telangiectasia/deficiência
Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Células Cultivadas
Macrófagos/imunologia
Macrófagos/virologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.1 (Atm protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170722
[St] Status:MEDLINE


  5 / 486 MEDLINE  
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[PMID]:28701397
[Au] Autor:Darrah EJ; Kulinski JM; Mboko WP; Xin G; Malherbe LP; Gauld SB; Cui W; Tarakanova VL
[Ad] Endereço:Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
[Ti] Título:B Cell-Specific Expression of Ataxia-Telangiectasia Mutated Protein Kinase Promotes Chronic Gammaherpesvirus Infection.
[So] Source:J Virol;91(19), 2017 Oct 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Manipulation of host cellular pathways is a strategy employed by gammaherpesviruses, including mouse gammaherpesvirus 68 (MHV68), in order to negotiate a chronic infection. Ataxia-telangiectasia mutated (ATM) plays a unique yet incompletely understood role in gammaherpesvirus infection, as it has both proviral and antiviral effects. Chronic gammaherpesvirus infection is poorly controlled in a host with global ATM insufficiency, whether the host is a mouse or a human. In contrast, ATM facilitates replication, reactivation, and latency establishment of several gammaherpesviruses , suggesting that ATM is proviral in the context of infected cell cultures. The proviral role of ATM is also evident , as myeloid-specific ATM expression facilitates MHV68 reactivation during the establishment of viral latency. In order to better understand the complex relationship between host ATM and gammaherpesvirus infection, we depleted ATM specifically in B cells, a cell type critical for chronic gammaherpesvirus infection. B cell-specific ATM deficiency attenuated the establishment of viral latency due to compromised differentiation of ATM-deficient B cells. Further, we found that during long-term infection, peritoneal B-1b, but not related B-1a, B cells display the highest frequency of gammaherpesvirus infection. While ATM expression did not affect gammaherpesvirus tropism for B-1 B cells, B cell-specific ATM expression was necessary to support viral reactivation from peritoneal cells during long-term infection. Thus, our study reveals a role of ATM as a host factor that promotes chronic gammaherpesvirus infection of B cells. Gammaherpesviruses infect a majority of the human population and are associated with cancer, including B cell lymphomas. ATM is a unique host kinase that has both proviral and antiviral roles in the context of gammaherpesvirus infection. Further, there is insufficient understanding of the interplay of these roles during chronic infection. In this study, we show that ATM expression by splenic B cells is required for efficient establishment of gammaherpesvirus latency. We also show that ATM expression by peritoneal B cells is required to facilitate viral reactivation during long-term infection. Thus, our study defines a proviral role of B cell-specific ATM expression during chronic gammaherpesvirus infection.
[Mh] Termos MeSH primário: Linfócitos B/metabolismo
Infecções por Herpesviridae/virologia
Rhadinovirus/crescimento & desenvolvimento
Ativação Viral/fisiologia
Latência Viral/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas Mutadas de Ataxia Telangiectasia/biossíntese
Proteínas Mutadas de Ataxia Telangiectasia/deficiência
Proteínas Mutadas de Ataxia Telangiectasia/genética
Linfócitos B/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Linhagem Celular
Infecções por Herpesviridae/imunologia
Interações Hospedeiro-Patógeno/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Peritônio/citologia
Peritônio/imunologia
Rhadinovirus/imunologia
Baço/citologia
Baço/imunologia
Ativação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins); EC 2.7.11.1 (Atm protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE


  6 / 486 MEDLINE  
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[PMID]:28689040
[Au] Autor:Liu M; Barton ES; Jennings RN; Oldenburg DG; Whirry JM; White DW; Grayson JM
[Ad] Endereço:Department of Microbiology and Immunology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA.
[Ti] Título:Unsupervised learning techniques reveal heterogeneity in memory CD8 T cell differentiation following acute, chronic and latent viral infections.
[So] Source:Virology;509:266-279, 2017 Sep.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD8 T lymphocytes are critical for the control of gammaherpesvirus latency. To determine how memory CD8 T cells generated during latency differ from those primed during acute or chronic viral infection, we adoptively transferred naive P14 CD8 T cells into uninfected recipients, and examined surface proteins, cytokines and transcription factors following infection with the Armstrong (acute) or Clone 13 (chronic) strains of lymphocytic choriomeningitis virus (LCMV), or murine gammaherpesvirus 68 (MHV68) expressing the LCMV epitope D GP33-41. By performing k-means clustering and generating self organizing maps (SOM), we observed increased short-lived effector-like, CD27 CD62L and Bcl-6 CD8 T cells following latent infection. In addition, we found that memory CD8 T cells from latent primed mice underwent less expansion following adoptive transfer and antigen rechallenge. Data from cluster models were combined and visualized by principal component analysis (PCA) demonstrating memory CD8 T cells from latent infection occupy an intermediate differentiation space.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Memória Imunológica
Vírus da Coriomeningite Linfocítica/imunologia
Rhadinovirus/imunologia
Subpopulações de Linfócitos T/imunologia
Viroses/imunologia
Viroses/patologia
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD8-Positivos/química
Linfócitos T CD8-Positivos/classificação
Doença Crônica
Aprendizado de Máquina
Camundongos
Subpopulações de Linfócitos T/química
Subpopulações de Linfócitos T/classificação
Latência Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170721
[Lr] Data última revisão:
170721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170710
[St] Status:MEDLINE


  7 / 486 MEDLINE  
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[PMID]:28615210
[Au] Autor:Loftus MS; Verville N; Kedes DH
[Ad] Endereço:Department of Microbiology, Immunology, and Cancer Biology, University of Virginia, Charlottesville, Virginia, USA.
[Ti] Título:A Conserved Leucine Zipper Motif in Gammaherpesvirus ORF52 Is Critical for Distinct Microtubule Rearrangements.
[So] Source:J Virol;91(17), 2017 Sep 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Productive viral infection often depends on the manipulation of the cytoskeleton. Herpesviruses, including rhesus monkey rhadinovirus (RRV) and its close homolog, the oncogenic human gammaherpesvirus Kaposi's sarcoma-associated herpesvirus/human herpesvirus 8 (KSHV/HHV8), exploit microtubule (MT)-based retrograde transport to deliver their genomes to the nucleus. Subsequently, during the lytic phase of the life cycle, the maturing viral particles undergo orchestrated translocation to specialized regions within the cytoplasm, leading to tegumentation, secondary envelopment, and then egress. As a result, we hypothesized that RRV might induce changes in the cytoskeleton at both early and late stages of infection. Using confocal imaging, we found that RRV infection led to the thickening and acetylation of MTs emanating from the MT-organizing center (MTOC) shortly after viral entry and more pronounced and diffuse MT reorganization during peak stages of lytic gene expression and virion production. We subsequently identified open reading frame 52 (ORF52), a multifunctional and abundant tegument protein, as being the only virally encoded component responsible for these cytoskeletal changes. Mutational and modeling analyses indicated that an evolutionarily conserved, truncated leucine zipper motif near the N terminus as well as a strictly conserved arginine residue toward the C terminus of ORF52 play critical roles in its ability to rearrange the architecture of the MT cytoskeleton. Taken together, our findings combined with data from previous studies describing diverse roles for ORF52 suggest that it likely binds to different cellular components, thereby allowing context-dependent modulation of function. A thorough understanding of the processes governing viral infection includes knowledge of how viruses manipulate their intracellular milieu, including the cytoskeleton. Altering the dynamics of actin or MT polymerization, for example, is a common strategy employed by viruses to ensure efficient entry, maturation, and egress as well as the avoidance of antiviral defenses through the sequestration of key cellular factors. We found that infection with RRV, a homolog of the human pathogen KSHV, led to perinuclear wrapping by acetylated MT bundles and identified ORF52 as the viral protein underlying these changes. Remarkably, incoming virions were able to supply sufficient ORF52 to induce MT thickening and acetylation near the MTOC, potentially aiding in the delivery viral genomes to the nucleus. Although the function of MT alterations during late stages of infection requires further study, ORF52 shares functional and structural similarities with alphaherpesvirus VP22, underscoring the evolutionary importance of MT cytoskeletal manipulations for this virus family.
[Mh] Termos MeSH primário: Zíper de Leucina
Centro Organizador dos Microtúbulos/metabolismo
Microtúbulos/metabolismo
Rhadinovirus/genética
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Núcleo Celular/virologia
Fibroblastos/virologia
Zíper de Leucina/genética
Macaca mulatta
Centro Organizador dos Microtúbulos/virologia
Microtúbulos/virologia
Fases de Leitura Aberta
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE


  8 / 486 MEDLINE  
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[PMID]:28424280
[Au] Autor:Zeippen C; Javaux J; Xiao X; Ledecq M; Mast J; Farnir F; Vanderplasschen A; Stevenson P; Gillet L
[Ad] Endereço:Immunology-Vaccinology, Department of Infectious and Parasitic Diseases, Faculty of Veterinary Medicine-Fundamental and Applied Research for Animals and Health (FARAH), University of Liège, Liège, Belgium.
[Ti] Título:The Major Envelope Glycoprotein of Murid Herpesvirus 4 Promotes Sexual Transmission.
[So] Source:J Virol;91(13), 2017 Jul 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gammaherpesviruses are important human and animal pathogens. Infection control has proven difficult because the key process of transmission is ill understood. Murid herpesvirus 4 (MuHV-4), a gammaherpesvirus of mice, is transmitted sexually. We show that this depends on the major virion envelope glycoprotein gp150. gp150 is redundant for host entry, and , it regulates rather than promotes cell binding. We show that gp150-deficient MuHV-4 reaches and replicates normally in the female genital tract after nasal infection but is poorly released from vaginal epithelial cells and fails to pass from the female to the male genital tract during sexual contact. Thus, we show that the regulation of virion binding is a key component of spontaneous gammaherpesvirus transmission. Gammaherpesviruses are responsible for many important diseases in both animals and humans. Some important aspects of their life cycle are still poorly understood. Key among these is viral transmission. Here we show that the major envelope glycoprotein of murid herpesvirus 4 functions not in entry or dissemination but in virion release to allow sexual transmission to new hosts.
[Mh] Termos MeSH primário: Glicoproteínas/metabolismo
Infecções por Herpesviridae/veterinária
Rhadinovirus/fisiologia
Doenças Virais Sexualmente Transmissíveis/veterinária
Proteínas do Envelope Viral/metabolismo
Liberação de Vírus
[Mh] Termos MeSH secundário: Animais
Transmissão de Doença Infecciosa
Glicoproteínas/genética
Infecções por Herpesviridae/transmissão
Infecções por Herpesviridae/virologia
Doenças Virais Sexualmente Transmissíveis/transmissão
Doenças Virais Sexualmente Transmissíveis/virologia
Proteínas do Envelope Viral/genética
Ligação Viral
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE


  9 / 486 MEDLINE  
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[PMID]:28394921
[Au] Autor:Tan CSE; Lawler C; Stevenson PG
[Ad] Endereço:School of Chemistry and Molecular Biosciences, University of Queensland and Royal Children's Hospital, Brisbane, Australia.
[Ti] Título:CD8+ T cell evasion mandates CD4+ T cell control of chronic gamma-herpesvirus infection.
[So] Source:PLoS Pathog;13(4):e1006311, 2017 Apr.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gamma-herpesvirus infections are regulated by both CD4+ and CD8+ T cells. However clinical disease occurs mainly in CD4+ T cell-deficient hosts. In CD4+ T cell-deficient mice, CD8+ T cells control acute but not chronic lung infection by Murid Herpesvirus-4 (MuHV-4). We show that acute and chronic lung infections differ in distribution: most acute infection was epithelial, whereas most chronic infection was in myeloid cells. CD8+ T cells controlled epithelial infection, but CD4+ T cells and IFNγ were required to control myeloid cell infection. Disrupting the MuHV-4 K3, which degrades MHC class I heavy chains, increased viral epitope presentation by infected lung alveolar macrophages and allowed CD8+ T cells to prevent disease. Thus, viral CD8+ T cell evasion led to niche-specific immune control, and an essential role for CD4+ T cells in limiting chronic infection.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Infecções por Herpesviridae/imunologia
Infecções por Herpesviridae/virologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Antígenos de Histocompatibilidade Classe I/imunologia
Camundongos
Camundongos Knockout
Rhadinovirus/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006311


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[PMID]:28334904
[Au] Autor:Karijolich J; Zhao Y; Alla R; Glaunsinger B
[Ad] Endereço:Howard Hughes Medical Institute, University of California, Berkeley, CA 94720-3370, USA.
[Ti] Título:Genome-wide mapping of infection-induced SINE RNAs reveals a role in selective mRNA export.
[So] Source:Nucleic Acids Res;45(10):6194-6208, 2017 Jun 02.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Short interspersed nuclear elements (SINEs) are retrotransposons evolutionarily derived from endogenous RNA Polymerase III RNAs. Though SINE elements have undergone exaptation into gene regulatory elements, how transcribed SINE RNA impacts transcriptional and post-transcriptional regulation is largely unknown. This is partly due to a lack of information regarding which of the loci have transcriptional potential. Here, we present an approach (short interspersed nuclear element sequencing, SINE-seq), which selectively profiles RNA Polymerase III-derived SINE RNA, thereby identifying transcriptionally active SINE loci. Applying SINE-seq to monitor murine B2 SINE expression during a gammaherpesvirus infection revealed transcription from 28 270 SINE loci, with ∼50% of active SINE elements residing within annotated RNA Polymerase II loci. Furthermore, B2 RNA can form intermolecular RNA-RNA interactions with complementary mRNAs, leading to nuclear retention of the targeted mRNA via a mechanism involving p54nrb. These findings illuminate a pathway for the selective regulation of mRNA export during stress via retrotransposon activation.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/genética
RNA Mensageiro/genética
Elementos Nucleotídeos Curtos e Dispersos/genética
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/genética
Proteínas de Ciclo Celular/genética
Técnicas de Silenciamento de Genes
Infecções por Herpesviridae/genética
Camundongos
Células NIH 3T3
Proteínas Associadas à Matriz Nuclear/metabolismo
Interferência de RNA
RNA Polimerase III/genética
RNA Mensageiro/metabolismo
Proteínas de Ligação a RNA/metabolismo
Retroelementos/fisiologia
Rhadinovirus
Análise de Sequência de DNA
Estresse Fisiológico/genética
Frações Subcelulares/metabolismo
Transcrição Genética
Infecções Tumorais por Vírus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Nuclear Matrix-Associated Proteins); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Retroelements); 0 (SGOL2 protein, mouse); 0 (p54nrb protein, mouse); EC 2.7.7.6 (RNA Polymerase III)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx180



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