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[PMID]:28464285
[Au] Autor:Huang H; Zhang N; Xiong Q; Chen R; Zhang C; Wang N; Wang L; Ren H; Liu M; Qian M; Du B
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
[Ti] Título:Elimination of GPR146-mediated antiviral function through IRF3/HES1-signalling pathway.
[So] Source:Immunology;152(1):102-114, 2017 09.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:As the most important host defence against viral infection, interferon (IFN) stimulates hundreds of antiviral genes (ISGs) that together establish an 'antiviral state'. However, the antiviral function of most ISGs in viral infection still need further exploration. Here, we demonstrated that the expression of G-protein-coupled receptor 146 (GPR146) is highly increased by both IFN-ß and IFN-γ in a signal transducer and activator of transcription 1-dependent signalling pathway. Most importantly, overexpression of GPR146 protects the host cells from vesicular stomatitis virus and Newcastle disease virus infection but not from infection by herpes simplex virus. In contrast, the virus-induced IFN-ß production changed little in Gpr146-knockout cells. Furthermore, the Gpr146-deficient mice showed similar susceptibility to wild-type mice with vesicular stomatitis virus infection. Interestingly, the expression of GPR146 in virus-infected cells was strikingly reduced and can partially explain why the viral infection was little influenced in Gpr146-knockout mice. Surprisingly, virus-activated IFN regulatory factor 3 (IRF3) signalling not only induces the expression of IFN but also represses GPR146 expression through HES1 (hairy and enhancer of split-1)-mediated transcriptional activity to establish a dynamic equilibrium between pro-viral and antiviral stages in host cells. Taken together, these data reveal the antiviral role of GPR146 in fighting viral infection although the GPR146-mediated protection is eliminated by IRF3/HES1-signalling, which suggests a potential therapeutic significance of both GPR146 and HES1 signalling in viral infection.
[Mh] Termos MeSH primário: Herpes Simples/prevenção & controle
Fator Regulador 3 de Interferon/metabolismo
Macrófagos Peritoneais/metabolismo
Doença de Newcastle/prevenção & controle
Receptores Acoplados a Proteínas-G/deficiência
Transdução de Sinais
Fatores de Transcrição HES-1/metabolismo
Estomatite Vesicular/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Cercopithecus aethiops
Genótipo
Células HEK293
Herpes Simples/imunologia
Herpes Simples/metabolismo
Herpes Simples/virologia
Herpesvirus Humano 1/imunologia
Herpesvirus Humano 1/metabolismo
Interações Hospedeiro-Patógeno
Seres Humanos
Fator Regulador 3 de Interferon/imunologia
Interferon beta/farmacologia
Interferon gama/farmacologia
Macrófagos Peritoneais/efeitos dos fármacos
Macrófagos Peritoneais/imunologia
Macrófagos Peritoneais/virologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Doença de Newcastle/imunologia
Doença de Newcastle/metabolismo
Doença de Newcastle/virologia
Vírus da Doença de Newcastle/imunologia
Vírus da Doença de Newcastle/metabolismo
Fenótipo
Células RAW 264.7
Interferência de RNA
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/imunologia
Fatores de Transcrição HES-1/imunologia
Transfecção
Células Vero
Estomatite Vesicular/imunologia
Estomatite Vesicular/metabolismo
Estomatite Vesicular/virologia
Vírus da Estomatite Vesicular Indiana/imunologia
Vírus da Estomatite Vesicular Indiana/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (G protein-coupled receptor 146, mouse); 0 (Hes1 protein, mouse); 0 (IFNG protein, mouse); 0 (Interferon Regulatory Factor-3); 0 (Irf3 protein, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Transcription Factor HES-1); 77238-31-4 (Interferon-beta); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12752


  2 / 5215 MEDLINE  
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[PMID]:29242538
[Au] Autor:Liu S; Jiang M; Wang W; Liu W; Song X; Ma Z; Zhang S; Liu L; Liu Y; Cao X
[Ad] Endereço:Department of Immunology & Centre for Immunotherapy, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
[Ti] Título:Nuclear RNF2 inhibits interferon function by promoting K33-linked STAT1 disassociation from DNA.
[So] Source:Nat Immunol;19(1):41-52, 2018 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prolonged activation of interferon-STAT1 signaling is closely related to inflammatory autoimmune disorders, and therefore the identification of negative regulators of these pathways is important. Through high-content screening of 115 mouse RING-domain E3 ligases, we identified the E3 ubiquitin ligase RNF2 as a potent inhibitor of interferon-dependent antiviral responses. RNF2 deficiency substantially enhanced interferon-stimulated gene (ISG) expression and antiviral responses. Mechanistically, nuclear RNF2 directly bound to STAT1 after interferon stimulation and increased K33-linked polyubiquitination of the DNA-binding domain of STAT1 at position K379, in addition to promoting the disassociation of STAT1/STAT2 from DNA and consequently suppressing ISG transcription. Our study provides insight into the regulation of interferon-dependent responses via a previously unrecognized post-translational modification of STAT1 in the nucleus.
[Mh] Termos MeSH primário: DNA/metabolismo
Interferon Tipo I/farmacologia
Lisina/metabolismo
Complexo Repressor Polycomb 1/metabolismo
Fator de Transcrição STAT1/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Antivirais/farmacologia
Linhagem Celular
Expressão Gênica/efeitos dos fármacos
Lisina/genética
Macrófagos/metabolismo
Macrófagos/virologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Complexo Repressor Polycomb 1/genética
Ligação Proteica/efeitos dos fármacos
Fator de Transcrição STAT1/genética
Fator de Transcrição STAT2/genética
Fator de Transcrição STAT2/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitinação/efeitos dos fármacos
Estomatite Vesicular/genética
Estomatite Vesicular/prevenção & controle
Estomatite Vesicular/virologia
Vírus da Estomatite Vesicular Indiana/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Interferon Type I); 0 (STAT1 Transcription Factor); 0 (STAT2 Transcription Factor); 9007-49-2 (DNA); EC 2.3.2.27 (Polycomb Repressive Complex 1); EC 2.3.2.27 (Rnf2 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1038/s41590-017-0003-0


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[PMID]:28687662
[Au] Autor:Zhang C; He H; Wang L; Zhang N; Huang H; Xiong Q; Yan Y; Wu N; Ren H; Han H; Liu M; Qian M; Du B
[Ad] Endereço:Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai 200241, China; and.
[Ti] Título:Virus-Triggered ATP Release Limits Viral Replication through Facilitating IFN-ß Production in a P2X7-Dependent Manner.
[So] Source:J Immunol;199(4):1372-1381, 2017 Aug 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Accumulating evidence shows that innate immune responses are associated with extracellular nucleotides, particularly ATP. In this article, we demonstrate extensive protection of ATP/P2X7 signaling in a host against viral infection. Interestingly, we observed a significant increase in ATP as a danger signal in vesicular stomatitis virus (VSV)-infected cell supernatant and VSV-infected mice in an exocytosis- and pannexin channel-dependent manner. Furthermore, extracellular ATP reduces the replication of VSV, Newcastle disease virus, murine leukemia virus, and HSV in vivo and in vitro through the P2X7 receptor. Meanwhile, ATP significantly increases IFN-ß expression in a concentration- and time-dependent manner. Mechanistically, ATP facilitates IFN-ß secretion through P38/JNK/ATF-2 signaling pathways, which are crucial in promoting antiviral immunity. Taken together, these results demonstrate the protective role of extracellular ATP and P2X7 in viral infection and suggest a potential therapeutic role for ATP/P2X7 in viral diseases.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Interferon beta/biossíntese
Receptores Purinérgicos P2X7/metabolismo
Estomatite Vesicular/imunologia
Vírus da Estomatite Vesicular Indiana/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/farmacologia
Animais
Imunidade Inata
Interferon beta/genética
Interferon beta/imunologia
Vírus da Leucemia Murina/efeitos dos fármacos
Vírus da Leucemia Murina/imunologia
Medições Luminescentes
Camundongos
Vírus da Doença de Newcastle/efeitos dos fármacos
Vírus da Doença de Newcastle/imunologia
Células RAW 264.7
Receptores Purinérgicos P2X7/imunologia
Transdução de Sinais
Simplexvirus/efeitos dos fármacos
Simplexvirus/imunologia
Estomatite Vesicular/virologia
Vírus da Estomatite Vesicular Indiana/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/imunologia
Replicação Viral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Purinergic P2X7); 77238-31-4 (Interferon-beta); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700187


  4 / 5215 MEDLINE  
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[PMID]:28666733
[Au] Autor:Klimenko K; Lyakhov S; Shibinskaya M; Karpenko A; Marcou G; Horvath D; Zenkova M; Goncharova E; Amirkhanov R; Krysko A; Andronati S; Levandovskiy I; Polishchuk P; Kuz'min V; Varnek A
[Ad] Endereço:Laboratoire de Chemoinformatique, (UMR 7140 CNRS/UniStra), Université de Strasbourg, 4, rue B. Pascal, Strasbourg 67000, France; A.V. Bogatsky Physico-Chemical Institute of NAS of Ukraine, Lyustdorfskaya doroga, 86, Odessa 65080, Ukraine.
[Ti] Título:Virtual screening, synthesis and biological evaluation of DNA intercalating antiviral agents.
[So] Source:Bioorg Med Chem Lett;27(16):3915-3919, 2017 08 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This paper describes computer-aided design of new anti-viral agents against Vaccinia virus (VACV) potentially acting as nucleic acid intercalators. Earlier obtained experimental data for DNA intercalation affinities and activities against Vesicular stomatitis virus (VSV) have been used to build, respectively, pharmacophore and QSAR models. These models were used for virtual screening of a database of 245 molecules generated around typical scaffolds of known DNA intercalators. This resulted in 12 hits which then were synthesized and tested for antiviral activity against VaV together with 43 compounds earlier studied against VSV. Two compounds displaying high antiviral activity against VaV and low cytotoxicity were selected for further antiviral activity investigations.
[Mh] Termos MeSH primário: Antivirais/farmacologia
DNA/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antivirais/síntese química
Antivirais/química
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Seres Humanos
Testes de Sensibilidade Microbiana
Estrutura Molecular
Relação Quantitativa Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 9007-49-2 (DNA)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE


  5 / 5215 MEDLINE  
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[PMID]:28630358
[Au] Autor:ElSherif MS; Brown C; MacKinnon-Cameron D; Li L; Racine T; Alimonti J; Rudge TL; Sabourin C; Silvera P; Hooper JW; Kwilas SA; Kilgore N; Badorrek C; Ramsey WJ; Heppner DG; Kemp T; Monath TP; Nowak T; McNeil SA; Langley JM; Halperin SA; Canadian Immunization Research Network
[Ad] Endereço:Canadian Center for Vaccinology (ElSherif, Brown, MacKinnon-Cameron, Li, McNeil, Langley, Halperin), IWK Health Centre and Nova Scotia Health Authority, Dalhousie University, Halifax, NS; National Microbiology Laboratory (Racine, Alimonti), Winnipeg, Man.; Battelle Biomedical Research Center (Rudge,
[Ti] Título:Assessing the safety and immunogenicity of recombinant vesicular stomatitis virus Ebola vaccine in healthy adults: a randomized clinical trial.
[So] Source:CMAJ;189(24):E819-E827, 2017 Jun 19.
[Is] ISSN:1488-2329
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The 2013-2016 Ebola virus outbreak in West Africa was the most widespread in history. In response, alive attenuated recombinant vesicular stomatitis virus (rVSV) vaccine expressing glycoprotein (rVSVΔG-ZEBOV-GP) was evaluated in humans. METHODS: In a phase 1, randomized, dose-ranging, observer-blind, placebo-controlled trial, healthy adults aged 18-65 years were randomized into 4 groups of 10 to receive one of 3 vaccine doses or placebo. Follow-up visits spanned 180 days postvaccination for safety monitoring, immunogenicity testing and any rVSV virus shedding. RESULTS: Forty participants were injected with rVSVΔG-ZEBOV-GP vaccine ( = 30) or saline placebo ( = 10). No serious adverse events related to the vaccine or participant withdrawals were reported. Solicited adverse events during the 14-day follow-up period were mild to moderate and self-limited, with the exception of injection-site pain and headache. Viremia following vaccination was transient and no longer detectable after study day 3, with no virus shedding in saliva or urine. All vaccinated participants developed serum immunoglobulin G (IgG), as measured by Ebola virus envelope glycoprotein-based enzyme-linked immunosorbent assay (ELISA). Immunogenicity was comparable across all dose groups, and sustained IgG titers were detectable through to the last visit, at study day 180. INTERPRETATION: In this phase 1 study, there were no safety concerns after a single dose of rVSVΔG-ZEBOV-GP vaccine. IgG ELISA showed persistent high titers at 180 days postimmunization. There was a period of reactogenicity, but in general, the vaccine was well tolerated. This study provides evidence of the safety and immunogenicity of rVSVΔG-ZEBOV-GP vaccine and importance of its further investigation. Clinical-Trials.gov no., NCT02374385.
[Mh] Termos MeSH primário: Vacinas contra Ebola/administração & dosagem
Doença pelo Vírus Ebola/prevenção & controle
Glicoproteínas de Membrana/imunologia
Proteínas do Envelope Viral/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Anticorpos Neutralizantes/sangue
Anticorpos Antivirais/sangue
Canadá
Método Duplo-Cego
Ebolavirus
Feminino
Voluntários Saudáveis
Seres Humanos
Imunoglobulina G/sangue
Masculino
Glicoproteínas de Membrana/genética
Meia-Idade
Análise de Regressão
Vacinação/métodos
Vacinas Sintéticas/administração & dosagem
Vírus da Estomatite Vesicular Indiana
Proteínas do Envelope Viral/genética
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (Ebola Vaccines); 0 (G protein, vesicular stomatitis virus); 0 (Immunoglobulin G); 0 (Membrane Glycoproteins); 0 (Vaccines, Synthetic); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1503/cmaj.170074


  6 / 5215 MEDLINE  
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[PMID]:28514874
[Au] Autor:Velazquez-Salinas L; Naik S; Pauszek SJ; Peng KW; Russell SJ; Rodriguez LL
[Ad] Endereço:1 United States Department of Agriculture, Agricultural Research Services , Foreign Animal Disease Research Unit, Plum Island, New York.
[Ti] Título:Oncolytic Recombinant Vesicular Stomatitis Virus (VSV) Is Nonpathogenic and Nontransmissible in Pigs, a Natural Host of VSV.
[So] Source:Hum Gene Ther Clin Dev;28(2):108-115, 2017 Jun.
[Is] ISSN:2324-8645
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vesicular stomatitis virus (VSV) is a negative-stranded RNA virus that naturally causes disease in livestock including horses, cattle and pigs. The two main identified VSV serotypes are New Jersey (VSNJV) and Indiana (VSIV). VSV is a rapidly replicating, potently immunogenic virus that has been engineered to develop novel oncolytic therapies for cancer treatment. Swine are a natural host for VSV and provide a relevant and well-established model, amenable to biological sampling to monitor virus shedding and neutralizing antibodies. Previous reports have documented the pathogenicity and transmissibility of wild-type isolates and recombinant strains of VSIV and VSNJV using the swine model. Oncolytic VSV engineered to express interferon-beta (IFNß) and the sodium iodide symporter (NIS), VSV-IFNß-NIS, has been shown to be a potent new therapeutic agent inducing rapid and durable tumor remission following systemic therapy in preclinical mouse models. VSV-IFNß-NIS is currently undergoing clinical evaluation for the treatment of advanced cancer in human and canine patients. To support clinical studies and comprehensively assess the risk of transmission to susceptible species, we tested the pathogenicity and transmissibility of oncolytic VSV-IFNß-NIS using the swine model. Following previously established protocols to evaluate VSV pathogenicity, intradermal inoculation with 10 TCID VSV-IFNß-NIS caused no observable symptoms in pigs. There was no detectable shedding of infectious virus in VSV-IFNß-NIS in biological excreta of inoculated pigs or exposed naive pigs kept in direct contact throughout the experiment. VSV-IFNß-NIS inoculated pigs became seropositive for VSV antibodies, while contact pigs displayed no symptoms of VSV infection, and importantly did not seroconvert. These data indicate that oncolytic VSV is both nonpathogenic and not transmissible in pigs, a natural host. These findings support further clinical development of oncolytic VSV-IFNß-NIS as a safe therapeutic for human and canine cancer.
[Mh] Termos MeSH primário: Terapia Viral Oncolítica/efeitos adversos
Vírus Oncolíticos/patogenicidade
Vírus da Estomatite Vesicular Indiana/patogenicidade
Vírus da Estomatite Vesicular New Jersey/patogenicidade
[Mh] Termos MeSH secundário: Animais
Interferon gama/genética
Interferon gama/metabolismo
Vírus Oncolíticos/genética
Suínos
Simportadores/genética
Simportadores/metabolismo
Vírus da Estomatite Vesicular Indiana/genética
Vírus da Estomatite Vesicular New Jersey/genética
Eliminação de Partículas Virais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Symporters); 0 (sodium-iodide symporter); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1089/humc.2017.015


  7 / 5215 MEDLINE  
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[PMID]:28381565
[Au] Autor:Liberatore RA; Mastrocola EJ; Powell C; Bieniasz PD
[Ad] Endereço:Aaron Diamond AIDS Research Center, New York, New York, USA.
[Ti] Título:Tetherin Inhibits Cell-Free Virus Dissemination and Retards Murine Leukemia Virus Pathogenesis.
[So] Source:J Virol;91(12), 2017 Jun 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The relative contributions of cell-free virion circulation and direct cell-to-cell transmission to retroviral dissemination and pathogenesis are unknown. Tetherin/Bst2 is an antiviral protein that blocks enveloped virion release into the extracellular milieu but may not inhibit cell-to-cell virus transmission. We developed live-cell imaging assays which show that tetherin does not affect Moloney murine leukemia virus (MoMLV) spread, and only minimally affects vesicular stomatitis virus (VSV) spread, to adjacent cells in a monolayer. Conversely, cell-free MLV and VSV virion yields and VSV spread to distal cells were dramatically reduced by tetherin. To elucidate the roles of tetherin and cell-free virions during viral dissemination and pathogenesis, we developed mice carrying an inducible human tetherin (hTetherin) transgene. While ubiquitous hTetherin expression was detrimental to the growth and survival of mice, restriction of hTetherin expression to hematopoietic cells gave apparently healthy mice. The expression of hTetherin in hematopoietic cells had little or no effect on the number of MoMLV-infected splenocytes and thymocytes. However, hTetherin expression significantly reduced cell-free plasma viremia and also delayed MoMLV-induced disease. Overall, these results suggest that MoMLV spread within hematopoietic tissues and cell monolayers involves cell-to-cell transmission that is resistant to tetherin but that virion dissemination via plasma is inhibited by tetherin and is required for full MoMLV pathogenesis. Retroviruses are thought to spread primarily via direct cell-to-cell transmission, yet many have evolved to counteract an antiviral protein called tetherin, which may selectively inhibit cell-free virus release. We generated a mouse model with an inducible tetherin transgene in order to study how tetherin affects retroviral dissemination and on which cell types its expression is required to do so. We first developed a novel live-cell imaging assay to demonstrate that while tetherin does indeed dramatically reduce cell-free virus spreading, it has little to no effect on direct cell-to-cell transmission of either vesicular stomatitis virus (VSV) or the retrovirus MoMLV. Using our transgenic mouse model, we found that tetherin expression on hematopoietic cells resulted in the specific reduction of MoMLV cell-free plasma viremia but not the number of infected hematopoietic cells. The delay in disease associated with this scenario suggests a role for cell-free virus in retroviral disease progression.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Vírus da Leucemia Murina de Moloney/fisiologia
Infecções por Retroviridae/virologia
Vírus da Estomatite Vesicular Indiana/fisiologia
Internalização do Vírus
Liberação de Vírus
[Mh] Termos MeSH secundário: Animais
Antígenos CD/genética
Antígenos CD/farmacologia
Proteínas Ligadas por GPI/genética
Proteínas Ligadas por GPI/metabolismo
Proteínas Ligadas por GPI/farmacologia
Células-Tronco Hematopoéticas/metabolismo
Células-Tronco Hematopoéticas/virologia
Seres Humanos
Camundongos
Camundongos Transgênicos
Células NIH 3T3
Baço/citologia
Baço/virologia
Timócitos/virologia
Viremia
Vírion/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (BST2 protein, human); 0 (GPI-Linked Proteins)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE


  8 / 5215 MEDLINE  
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[PMID]:28289159
[Au] Autor:Betancourt D; de Queiroz NM; Xia T; Ahn J; Barber GN
[Ad] Endereço:Department of Cell Biology, University of Miami Miller School of Medicine, Miami, FL 33136.
[Ti] Título:Cutting Edge: Innate Immune Augmenting Vesicular Stomatitis Virus Expressing Zika Virus Proteins Confers Protective Immunity.
[So] Source:J Immunol;198(8):3023-3028, 2017 Apr 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Zika virus (ZIKV) has become a serious public health concern because of its link to brain damage in developing human fetuses. Recombinant vesicular stomatitis virus (rVSV) was shown to be a highly effective and safe vector for the delivery of foreign immunogens for vaccine purposes. In this study, we generated rVSVs (wild-type and attenuated VSV with mutated matrix protein [VSVm] versions) that express either the full length ZIKV envelope protein (ZENV) alone or include the ZENV precursor to the membrane protein upstream of the envelope protein, and our rVSV-ZIKV constructs showed efficient immunogenicity in murine models. We also demonstrated maternal protective immunity in challenged newborn mice born to female mice vaccinated with VSVm-ZENV containing the transmembrane domain. Our data indicate that rVSVm may be a suitable strategy for the design of effective vaccines against ZIKV.
[Mh] Termos MeSH primário: Vetores Genéticos
Imunidade Inata/imunologia
Proteínas do Envelope Viral/imunologia
Vacinas Virais/imunologia
Infecção pelo Zika virus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Imunofluorescência
Seres Humanos
Immunoblotting
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Reação em Cadeia da Polimerase em Tempo Real
Vírus da Estomatite Vesicular Indiana/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Envelope Proteins); 0 (Viral Vaccines); 145420-18-4 (glycoprotein E, Flavivirus)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170315
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602180


  9 / 5215 MEDLINE  
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[PMID]:28237836
[Au] Autor:Shim KG; Zaidi S; Thompson J; Kottke T; Evgin L; Rajani KR; Schuelke M; Driscoll CB; Huff A; Pulido JS; Vile RG
[Ad] Endereço:Department of Molecular Medicine, Mayo Clinic, Rochester, MN 55905, USA; Medical Scientist Training Program, Mayo Clinic, Rochester, MN 55905, USA.
[Ti] Título:Inhibitory Receptors Induced by VSV Viroimmunotherapy Are Not Necessarily Targets for Improving Treatment Efficacy.
[So] Source:Mol Ther;25(4):962-975, 2017 Apr 05.
[Is] ISSN:1525-0024
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Systemic viroimmunotherapy activates endogenous innate and adaptive immune responses against both viral and tumor antigens. We have shown that therapy with vesicular stomatitis virus (VSV) engineered to express a tumor-associated antigen activates antigen-specific adoptively transferred T cells (adoptive cell therapy, ACT) in vivo to generate effective therapy. The overall goal of this study was to phenotypically characterize the immune response to VSV+ACT therapy and use the information gained to rationally improve combination therapy. We observed rapid expansion of blood CD8 effector cells acutely following VSV therapy with markedly high expression of the immune checkpoint molecules PD-1 and TIM-3. Using these data, we tested a treatment schedule incorporating mAb immune checkpoint inhibitors with VSV+ACT treatment. Unlike clinical scenarios, we delivered therapy at early time points following tumor establishment and treatment. Our goal was to potentiate the immune response generated by VSV therapy to achieve durable control of metastatic disease. Despite the high frequency of endogenous PD-1 TIM-3 CD8 T cells following virus administration, antibody blockade did not improve survival. These findings provide highly significant information about response kinetics to viroimmunotherapy and juxtapose the clinical use of checkpoint inhibitors against chronically dysfunctional T cells and the acute T cell response to oncolytic viruses.
[Mh] Termos MeSH primário: Transferência Adotiva
Antígenos de Neoplasias/genética
Antígenos de Neoplasias/imunologia
Vetores Genéticos/genética
Imunoterapia
Subpopulações de Linfócitos T/imunologia
Subpopulações de Linfócitos T/metabolismo
Vírus da Estomatite Vesicular Indiana/genética
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Receptor Celular 2 do Vírus da Hepatite A/antagonistas & inibidores
Receptor Celular 2 do Vírus da Hepatite A/metabolismo
Memória Imunológica
Melanoma Experimental/genética
Melanoma Experimental/imunologia
Melanoma Experimental/patologia
Melanoma Experimental/terapia
Camundongos
Mortalidade
Metástase Neoplásica
Receptor de Morte Celular Programada 1/antagonistas & inibidores
Receptor de Morte Celular Programada 1/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Havcr2 protein, mouse); 0 (Hepatitis A Virus Cellular Receptor 2); 0 (Programmed Cell Death 1 Receptor)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE


  10 / 5215 MEDLINE  
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[PMID]:28215695
[Au] Autor:Huangfu C; Ma Y; Jia J; Lv M; Zhu F; Ma X; Zhao X; Zhang J
[Ad] Endereço:Beijing Key Laboratory of Blood Safety and Supply Technologies, Beijing Institute of Transfusion Medicine, Beijing, 100850, China.
[Ti] Título:Inactivation of viruses by pasteurization at 60 °C for 10 h with and without 40% glucose as stabilizer during a new manufacturing process of α2-Macroglobulin from Cohn Fraction IV.
[So] Source:Biologicals;46:139-142, 2017 Mar.
[Is] ISSN:1095-8320
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pasteurization is regularly used to inactivate viruses for the safety of plasma derivatives. Influence of pasteurization at 60 °C for 10 h on α2-Macroglobulin activity and virus inactivation were studied. With 40% sugar as stabilizers more than 70% α2-Macroglobulin activity was reserved after pasteurization compared with 20% in control. Glucose presented a better activity protection effect than sucrose and maltose. By pasteurization without stabilizer the virus titers of pseudorabies virus, Sindbis virus, porcine parvovirus and encephalomyocarditis virus were reduced more than 5.88 log , 7.50 log , 4.88 log , and 5.63 log respectively within 2 h. By pasteurization with 40% glucose vesicular stomatitis virus was inactivated more than 5.88 log within 1 h. Only 2.71 log reduction was achieved for encephalomyocarditis virus after 10 h. 40% glucose protected α2-M activity and viruses simultaneously from pasteurization. Other viral inactivation methods need to be incorporated to ensure viral safety of this manufacturing process of α2-Macroglobulin.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Glucose/farmacologia
Temperatura Alta
Pasteurização/métodos
Inativação de Vírus/efeitos dos fármacos
alfa-Macroglobulinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Vírus da Encefalomiocardite/fisiologia
Herpesvirus Suídeo 1/fisiologia
Seres Humanos
Parvovirus Suíno/fisiologia
Reprodutibilidade dos Testes
Vírus Sindbis/fisiologia
Suínos
Fatores de Tempo
Células Vero
Vírus da Estomatite Vesicular Indiana/efeitos dos fármacos
Vírus da Estomatite Vesicular Indiana/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Proteins); 0 (Cohn fraction IV); 0 (alpha-Macroglobulins); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE



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