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[PMID]:29339251
[Au] Autor:Carta A; Sanna G; Briguglio I; Madeddu S; Vitale G; Piras S; Corona P; Peana AT; Laurini E; Fermeglia M; Pricl S; Serra A; Carta E; Loddo R; Giliberti G
[Ad] Endereço:Department of Chemistry and Pharmacy, University of Sassari, Via Muroni 23, 07100 Sassari, Italy. Electronic address: acarta@uniss.it.
[Ti] Título:Quinoxaline derivatives as new inhibitors of coxsackievirus B5.
[So] Source:Eur J Med Chem;145:559-569, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Enteroviruses are among the most common and important human pathogens for which there are no specific antiviral agents approved by the US Food and Drug Administration so far. Particularly, coxsackievirus infections have a worldwide distribution and can cause many important diseases. We here report the synthesis of new 14 quinoxaline derivatives and the evaluation of their cytotoxicity and antiviral activity against representatives of ssRNA, dsRNA and dsDNA viruses. Promisingly, three compounds showed a very potent and selective antiviral activity against coxsackievirus B5, with EC in the sub-micromolar range (0.3-0.06 µM). A combination of experimental techniques (i.e. virucidal activity, time of drug addition and adsorption assays) and in silico modeling studies were further performed, aiming to understand the mode of action of the most active, selective and not cytotoxic compound, the ethyl 4-[(2,3-dimethoxyquinoxalin-6-yl)methylthio]benzoate (6).
[Mh] Termos MeSH primário: Antivirais/farmacologia
Enterovirus Humano B/efeitos dos fármacos
Quinoxalinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Antivirais/síntese química
Antivirais/química
Bovinos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Cricetinae
Relação Dose-Resposta a Droga
Haplorrinos
Seres Humanos
Testes de Sensibilidade Microbiana
Modelos Moleculares
Estrutura Molecular
Quinoxalinas/síntese química
Quinoxalinas/química
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Quinoxalines)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:27773751
[Au] Autor:Pinkert S; Dieringer B; Diedrich S; Zeichhardt H; Kurreck J; Fechner H
[Ad] Endereço:Department of Applied Biochemistry, Institute of Biotechnology, Technische Universität Berlin, Berlin, Germany. Electronic address: sandra.pinkert@tu-berlin.de.
[Ti] Título:Soluble coxsackie- and adenovirus receptor (sCAR-Fc); a highly efficient compound against laboratory and clinical strains of coxsackie-B-virus.
[So] Source:Antiviral Res;136:1-8, 2016 12.
[Is] ISSN:1872-9096
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Coxsackie-B-viruses (CVB) cause a wide variety of diseases, ranging from mild syndromes to life-threatening conditions such as pancreatitis, myocarditis, meningitis and encephalitis. Especially newborns and young infants develop severe diseases and long-term sequelae may occur among survivors. Due to lack of specific antiviral therapy the current treatment of CVB infection is limited to symptomatic treatment. Here we analyzed the antiviral activity of a soluble receptor fusion protein, containing the extracellular part of the coxsackievirus and adenovirus receptor (CAR) fused to the constant domain of the human IgG - sCAR-Fc - against laboratory and clinical CVB strains. We found a high overall antiviral activity of sCAR-Fc against various prototypic laboratory strains of CVB, with an inhibition of viral replication up to 3 orders of magnitude (99.9%) at a concentration of 2.5 µg/ml. These include isolates that are not dependent on CAR for infection and isolates that are resistant against pleconaril, the currently most promising anti-CVB therapeutic. A complete inhibition was observed using higher concentration of sCAR-Fc. Further analysis of 23 clinical CVB isolates revealed overall high antiviral efficiency (up to 99.99%) of sCAR-Fc. In accordance with previous data, our results confirm the strong antiviral activity of sCAR-Fc against laboratory CVB strains and demonstrate for the first time that sCAR-Fc is also highly efficient at neutralizing clinical CVB isolates. Importantly, during the sCAR-Fc inhibition experiments, no naturally occurring resistant mutants were observed.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/química
Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/farmacologia
Enterovirus Humano B/efeitos dos fármacos
Imunoglobulina G/genética
[Mh] Termos MeSH secundário: Proteína de Membrana Semelhante a Receptor de Coxsackie e Adenovirus/genética
Infecções por Coxsackievirus/tratamento farmacológico
Infecções por Coxsackievirus/virologia
Células HeLa
Seres Humanos
Imunoglobulina G/farmacologia
Receptores de IgG
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/farmacologia
Solubilidade
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 (Coxsackie and Adenovirus Receptor-Like Membrane Protein); 0 (Immunoglobulin G); 0 (Receptors, IgG); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:29220410
[Au] Autor:Qiu Y; Ye X; Zhang HM; Hanson P; Zhao G; Tong L; Xie R; Yang D
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada.
[Ti] Título:Cleavage of osmosensitive transcriptional factor NFAT5 by Coxsackieviral protease 2A promotes viral replication.
[So] Source:PLoS Pathog;13(12):e1006744, 2017 Dec.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear factor of activated T cells 5 (NFAT5)/Tonicity enhancer binding protein (TonEBP) is a transcription factor induced by hypertonic stress in the kidney. However, the function of NFAT5 in other organs has rarely been studied, even though it is ubiquitously expressed. Indeed, although NFAT5 was reported to be critical for heart development and function, its role in infectious heart diseases has remained obscure. In this study, we aimed to understand the mechanism by which NFAT5 interferes with infection of Coxsackievirus B3 (CVB3), a major cause of viral myocarditis. Our initial results demonstrated that although the mRNA level of NFAT5 remained constant during CVB3 infection, NFAT5 protein level decreased because the protein was cleaved. Bioinformatic prediction and verification of the predicted site by site-directed mutagenesis experiments determined that the NFAT5 protein was cleaved by CVB3 protease 2A at Glycine 503. Such cleavage led to the inactivation of NFAT5, and the 70-kDa N-terminal cleavage product (p70-NFAT5) exerted a dominant negative effect on the full-length NFAT5 protein. We further showed that elevated expression of NFAT5 to counteract viral protease cleavage, especially overexpression of a non-cleavable mutant of NFAT5, significantly inhibited CVB3 replication. Ectopic expression of NFAT5 resulted in elevated expression of inducible nitric oxide synthase (iNOS), a factor reported to inhibit CVB3 replication. The necessity of iNOS for the anti-CVB3 effect of NFAT5 was supported by the observation that inhibition of iNOS blocked the anti-CVB3 effect of NFAT5. In a murine model of viral myocarditis, we observed that treatment with hypertonic saline or mannitol solution upregulated NFAT5 and iNOS expression, inhibited CVB3 replication and reduced tissue damage in the heart. Taken together, our data demonstrate that the anti-CVB3 activity of NFAT5 is impaired during CVB3 infection due to 2A-mediated cleavage of NFAT5. Thus induction of NFAT5 by hypertonic agents may be a promising strategy for the development of anti-CVB3 therapeutics.
[Mh] Termos MeSH primário: Infecções por Coxsackievirus/virologia
Cisteína Endopeptidases/metabolismo
Enterovirus Humano B/enzimologia
Miocardite/virologia
Miócitos Cardíacos/virologia
Fatores de Transcrição/metabolismo
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Linhagem Celular
Infecções por Coxsackievirus/imunologia
Infecções por Coxsackievirus/metabolismo
Infecções por Coxsackievirus/patologia
Enterovirus Humano B/imunologia
Enterovirus Humano B/fisiologia
Regulação da Expressão Gênica
Seres Humanos
Masculino
Camundongos Endogâmicos A
Mutação
Miocardite/imunologia
Miocardite/metabolismo
Miocardite/patologia
Miócitos Cardíacos/imunologia
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Óxido Nítrico Sintase Tipo II/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/química
Óxido Nítrico Sintase Tipo II/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Proteólise
Interferência de RNA
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Especificidade por Substrato
Fatores de Transcrição/antagonistas & inibidores
Fatores de Transcrição/química
Fatores de Transcrição/genética
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NFAT5 protein, human); 0 (Nfat5 protein, mouse); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Transcription Factors); 0 (Viral Proteins); EC 1.14.13.39 (NOS2 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.29 (picornain 2A, Picornavirus)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006744


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[PMID]:28973047
[Au] Autor:Sesti-Costa R; Françozo MCS; Silva GK; Proenca-Modena JL; Silva JS
[Ad] Endereço:Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
[Ti] Título:TLR3 is required for survival following Coxsackievirus B3 infection by driving T lymphocyte activation and polarization: The role of dendritic cells.
[So] Source:PLoS One;12(10):e0185819, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type B coxsackievirus (CVB) is a common cause of acute and chronic myocarditis, meningitis and pancreatitis, often leading to heart failure and pancreatic deficiency. The polarization of CD4+ T lymphocytes and their cytokine milieu are key factors in the outcome of CVB-induced diseases. Thus, sensing the virus and driving the adaptive immune response are essential for the establishment of a protective immune response. TLR3 is a crucial virus recognition receptor that confers the host with resistance to CVB infection. In the current study, we found that TLR3 expression in dendritic cells plays a role in their activation upon CVB3 infection in vitro, as TLR3-deficient dendritic cells up-regulate CD80 and CD86 to a less degree than WT cells. Instead, they up-regulated the inhibitory molecule PD-L1 and secreted considerably lower levels of TNF-α and IL-10 and a higher level of IL-23. T lymphocyte proliferation in co-culture with CVB3-infected dendritic cells was increased by TLR3-expressing DCs and other cells. Furthermore, in the absence of TLR3, the T lymphocyte response was shifted toward a Th17 profile, which was previously reported to be deleterious for the host. TLR3-deficient mice were very susceptible to CVB3 infection, with increased pancreatic injury and extensive inflammatory infiltrate in the heart that was associated with uncontrolled viral replication. Adoptive transfer of TLR3+ dendritic cells slightly improved the survival of TLR-deficient mice following CVB3 infection. Therefore, our findings highlight the importance of TLR3 signaling in DCs and in other cells to induce activation and polarization of the CD4+ T lymphocyte response toward a Th1 profile and consequently for a better outcome of CVB3 infection. These data provide new insight into the immune-mediated mechanisms by which CVBs are recognized and cleared in order to prevent the development of myocarditis and pancreatitis and may contribute to the design of therapies for enteroviral infections.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Infecções por Coxsackievirus/imunologia
Células Dendríticas/imunologia
Enterovirus Humano B
Ativação Linfocitária/fisiologia
Receptor 3 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos T CD4-Positivos/metabolismo
Infecções por Coxsackievirus/metabolismo
Citocinas/metabolismo
Células Dendríticas/metabolismo
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Toll-Like Receptor 3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185819


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[PMID]:28912259
[Au] Autor:Tschöpe C; Müller I; Xia Y; Savvatis K; Pappritz K; Pinkert S; Lassner D; Heimesaat MM; Spillmann F; Miteva K; Bereswill S; Schultheiss HP; Fechner H; Pieske B; Kühl U; Van Linthout S
[Ad] Endereço:From the Department of Cardiology and Pneumology, Charité-Universitätsmedizin Berlin, Campus Virchow Klinikum, Germany (C.T., Y.X., K.S., F.S., B.P., U.K., S.V.L.); DZHK (German Center for Cardiovascular Research), partner site Berlin, Germany (C.T., I.M., K.P., B.P., S.V.L.); Berlin-Brandenburg Cen
[Ti] Título:NOD2 (Nucleotide-Binding Oligomerization Domain 2) Is a Major Pathogenic Mediator of Coxsackievirus B3-Induced Myocarditis.
[So] Source:Circ Heart Fail;10(9), 2017 Sep.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The cytoplasmatic pattern recognition receptor, NOD2 (nucleotide-binding oligomerization domain 2), belongs to the innate immune system and is among others responsible for the recognition of single-stranded RNA. With Coxsackievirus B3 (CVB3) being a single-stranded RNA virus, and the recent evidence that the NOD2 target, NLRP3 (NOD-like receptor family, pyrin domain containing 3) is of importance in the pathogenesis of CVB3-induced myocarditis, we aimed to unravel the role of NOD2 in CVB3-induced myocarditis. METHODS AND RESULTS: Endomyocardial biopsy NOD2 mRNA expression was higher in CVB3-positive patients compared with patients with myocarditis but without evidence of persistent CVB3 infection. Left ventricular NOD2 mRNA expression was also induced in CVB3-induced myocarditis versus healthy control mice. NOD2 knockdown mice were rescued from the detrimental CVB3-mediated effects as shown by a reduced cardiac inflammation (less cardiac infiltrates and suppression of proinflammatory cytokines), cardiac fibrosis, apoptosis, lower CAR (Coxsackievirus and adenovirus receptor) expression and CVB3 copy number, and an improved left ventricular function in NOD2 CVB3 mice compared with wild-type CVB3 mice. In agreement, NOD2 decreased the CVB3-induced inflammatory response, CVB3 copy number, and apoptosis in vitro. NOD2 was further associated with a reduction in CVB3-induced NLRP3 expression and activity as evidenced by lower ASC (apoptosis-associated speck-like protein containing a CARD) expression, caspase 1 activity, or IL-1ß (interleukin-1ß) protein expression under in vivo and in vitro CVB3 conditions. CONCLUSIONS: NOD2 is an important mediator in the viral uptake and inflammatory response during the pathogenesis of CVB3 myocarditis.
[Mh] Termos MeSH primário: Infecções por Coxsackievirus/metabolismo
Enterovirus Humano B/metabolismo
Miocardite/metabolismo
Miocárdio/metabolismo
Proteína Adaptadora de Sinalização NOD2/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Proteínas Reguladoras de Apoptose/metabolismo
Proteínas Adaptadoras de Sinalização CARD
Estudos de Casos e Controles
Caspase 1/metabolismo
Linhagem Celular
Infecções por Coxsackievirus/imunologia
Infecções por Coxsackievirus/prevenção & controle
Infecções por Coxsackievirus/virologia
Modelos Animais de Doenças
Enterovirus Humano B/genética
Enterovirus Humano B/imunologia
Predisposição Genética para Doença
Interações Hospedeiro-Patógeno
Seres Humanos
Interleucina-1beta/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocardite/imunologia
Miocardite/prevenção & controle
Miocardite/virologia
Miocárdio/imunologia
Miocárdio/patologia
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Proteína Adaptadora de Sinalização NOD2/deficiência
Proteína Adaptadora de Sinalização NOD2/genética
Fenótipo
Interferência de RNA
Transdução de Sinais
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (CARD Signaling Adaptor Proteins); 0 (Card15 protein, mouse); 0 (IL1B protein, mouse); 0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NOD2 protein, human); 0 (Nlrp3 protein, mouse); 0 (Nod2 Signaling Adaptor Protein); 0 (Pycard protein, mouse); EC 3.4.22.36 (Caspase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


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[PMID]:28858766
[Au] Autor:Cao X; Wang W; Wang S; Bao L
[Ad] Endereço:College of Science, Huazhong Agricultural University, Wuhan 430070, People's Republic of China. Electronic address: caoxiufang@mail.hzau.edu.cn.
[Ti] Título:Asymmetric synthesis of novel triazole derivatives and their in vitro antiviral activity and mechanism of action.
[So] Source:Eur J Med Chem;139:718-725, 2017 Oct 20.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:In this study, forty-four chiral triazole derivatives have been prepared via asymmetric synthesis, and which has been successfully characterized by typical spectroscopic techniques including H NMR, C NMR, EI-MS, elemental analysis and optical rotations. Their in vitro antiviral activities against EV71 and CVB3 were fully investigated in cell-based assays. It was observed that 13 synthetic triazole derivatives inhibited the CPE of EV71 on RD cells, with EC in the 5.3-15.9 µg/ml range and corresponding SIs of 4.0-27.6, while 17 triazole derivatives showed antiviral activities against CVB3, with EC in the 4.7-15.1 µg/ml range and the corresponding SIs of 3.7-14.5. In addition, in some cases, the respective enantiomers showed significantly selective inhibitory effect against EV71, most notably for the enantiomers 9(R) and 10(S), 42(R) and 43(S), which presented an obvious activity difference. The most potential molecules are the compounds 10 and 43 with S-configuration, and which exhibit good SI values compared with the control Ribavirin.
[Mh] Termos MeSH primário: Antivirais/farmacologia
Enterovirus Humano B/efeitos dos fármacos
Triazóis/farmacologia
[Mh] Termos MeSH secundário: Antivirais/síntese química
Antivirais/química
Sobrevivência Celular
Relação Dose-Resposta a Droga
Seres Humanos
Testes de Sensibilidade Microbiana
Estrutura Molecular
Relação Estrutura-Atividade
Triazóis/síntese química
Triazóis/química
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Triazoles)
[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:170901
[St] Status:MEDLINE


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[PMID]:28800592
[Au] Autor:Müller I; Pappritz K; Savvatis K; Puhl K; Dong F; El-Shafeey M; Hamdani N; Hamann I; Noutsias M; Infante-Duarte C; Linke WA; Van Linthout S; Tschöpe C
[Ad] Endereço:Charité -Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Department of Internal Medicine and Cardiology, Campus Virchow Klinikum, Berlin, Germany.
[Ti] Título:CX3CR1 knockout aggravates Coxsackievirus B3-induced myocarditis.
[So] Source:PLoS One;12(8):e0182643, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Studies on inflammatory disorders elucidated the pivotal role of the CX3CL1/CX3CR1 axis with respect to the pathophysiology and diseases progression. Coxsackievirus B3 (CVB3)-induced myocarditis is associated with severe cardiac inflammation, which may progress to heart failure. We therefore investigated the influence of CX3CR1 ablation in the model of acute myocarditis, which was induced by inoculation with 5x105 plaque forming units of CVB3 (Nancy strain) in either CX3CR1-/- or C57BL6/j (WT) mice. Seven days after infection, myocardial inflammation, remodeling, and titin expression and phosphorylation were examined by immunohistochemistry, real-time PCR and Pro-Q diamond stain. Cardiac function was assessed by tip catheter. Compared to WT CVB3 mice, CX3CR1-/- CVB3 mice exhibited enhanced left ventricular expression of inflammatory cytokines and chemokines, which was associated with an increase of immune cell infiltration/presence. This shift towards a pro-inflammatory immune response further resulted in increased cardiac fibrosis and cardiomyocyte apoptosis, which was reflected by an impaired cardiac function in CX3CR1-/- CVB3 compared to WT CVB3 mice. These findings demonstrate a cardioprotective role of CX3CR1 in CVB3-infected mice and indicate the relevance of the CX3CL1/CX3CR1 system in CVB3-induced myocarditis.
[Mh] Termos MeSH primário: Quimiocina CX3CL1/imunologia
Infecções por Coxsackievirus/genética
Enterovirus Humano B/patogenicidade
Interações Hospedeiro-Patógeno/imunologia
Miocardite/genética
Receptores de Quimiocinas/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Receptor 1 de Quimiocina CX3C
Moléculas de Adesão Celular/genética
Moléculas de Adesão Celular/imunologia
Quimiocina CX3CL1/genética
Infecções por Coxsackievirus/imunologia
Infecções por Coxsackievirus/patologia
Infecções por Coxsackievirus/virologia
Modelos Animais de Doenças
Enterovirus Humano B/crescimento & desenvolvimento
Regulação da Expressão Gênica
Testes de Função Cardíaca
Seres Humanos
Interleucinas/genética
Interleucinas/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocardite/imunologia
Miocardite/patologia
Miocardite/virologia
Miócitos Cardíacos/imunologia
Miócitos Cardíacos/patologia
Fosforilação
Proteínas Quinases/genética
Proteínas Quinases/imunologia
Receptores de Quimiocinas/deficiência
Receptores de Quimiocinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cell Adhesion Molecules); 0 (Chemokine CX3CL1); 0 (Cx3cl1 protein, mouse); 0 (Cx3cr1 protein, mouse); 0 (Interleukins); 0 (Receptors, Chemokine); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (titin protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182643


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[PMID]:28766058
[Au] Autor:Svyatchenko VA; Ternovoy VA; Kiselev NN; Demina AV; Loktev VB; Netesov SV; Chumakov PM
[Ad] Endereço:State Research Center of Virology and Biotechnology "Vector", Koltsovo, Novosibirsk, Russia.
[Ti] Título:Bioselection of coxsackievirus B6 strain variants with altered tropism to human cancer cell lines.
[So] Source:Arch Virol;162(11):3355-3362, 2017 Nov.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:Cancer cells develop increased sensitivity to members of many virus families and, in particular, can be efficiently infected and lysed by many low-pathogenic human enteroviruses. However, because of their great genetic heterogeneity, cancer cells display different levels of sensitivity to particular enterovirus strains, which may substantially limit the chances of a positive clinical response. We show that a non-pathogenic strain of coxsackievirus B6 (LEV15) can efficiently replicate to high titers in the malignant human cell lines C33A, DU145, AsPC-1 and SK-Mel28, although it displays much lower replication efficiency in A431 and A549 cells and very limited replication ability in RD and MCF7 cells, as well as in the normal lung fibroblast cell line MRC-5 and the immortalized mammary epithelial cell line MCF10A. By serial passaging in RD, MCF7 and A431 cells, we obtained LEV15 strain variants that had acquired high replication capacity in the appropriate carcinoma cell lines without losing their high replication capability in the original set of cancer cell lines and had limited replication capability in untransformed cells. The strains demonstrated improved oncolytic properties in nude-mouse xenografts. We identified nucleotide changes responsible for the phenotypes and suggest a bioselection approach for a generation of oncolytic virus strains with a wider spectrum of affected tumors.
[Mh] Termos MeSH primário: Enterovirus Humano B/genética
Seleção Genética
Tropismo Viral/genética
Tropismo Viral/fisiologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Genoma Viral
Seres Humanos
Camundongos
Camundongos Nus
Neoplasias Experimentais
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3492-0


  9 / 4296 MEDLINE  
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[PMID]:28738914
[Au] Autor:Angez M; Shaukat S; Zahra R; Alam MM; Sharif S; Khurshid A; Arshad Y; Suleman M; Mujtaba G; Zaidi SSZ
[Ad] Endereço:Department of Virology,National Institute of Health,Chak Shahzad,Park Road,Islamabad-45500,Pakistan.
[Ti] Título:Characterization of group B coxsackieviruses isolated from non-polio acute flaccid paralysis patients in Pakistan: vital assessment before polio eradication.
[So] Source:Epidemiol Infect;145(12):2473-2481, 2017 09.
[Is] ISSN:1469-4409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pakistan is at the verge of polio eradication but isolation of non-polio enteroviruses (NPEVs) from acute flaccid paralysis (AFP) cases may result in serious or even fatal outcome. Many enteroviruses share similar symptoms and epidemiology as is the case with poliovirus and coxsackievirus (CV). The present study was designed to genetically characterize coxsackievirus B (CV-B) serotypes isolated from non-polio acute flaccid paralytic children, as well as to understand their probable role in paralysis. A total of 63 (20·1%) out of 313 stool samples during 2013 were found positive for NPEVs in rhabdomyosarcoma cells. Only 24 (38·0%) NPEVs were typed as CV-B by microneutralization assay and were further characterized by sequencing of the viral protein 1 (VP1) gene. Molecular phylogenetic analyses classified the study strains into six coxsackievirus B serotypes (coxsackievirus B1 to B6) with their respective prototype strains with evidence of epidemiological linkage and distinct clusters. Moreover, four major differences were found within the amino acid sequences of BC-loop in VP1 of CV-B strains. In conclusion, this study presented the molecular evolutionary genetic overview and distinct phylogenetic pattern of CV-B isolates from AFP cases in Pakistan, and explored the possible link between CV-B infections and AFP cases. Furthermore, our data reveal that these viruses might contribute to the incidence of paralysis in population and there is need of time to establish an enterovirus surveillance system for better understanding of epidemiological and virological characteristics of NPEV infections associated with AFP cases in the country.
[Mh] Termos MeSH primário: Proteínas do Capsídeo/genética
Infecções por Coxsackievirus/epidemiologia
Enterovirus Humano B/genética
Paralisia/epidemiologia
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Infecções por Coxsackievirus/virologia
Erradicação de Doenças
Enterovirus Humano B/classificação
Fezes/virologia
Feminino
Seres Humanos
Lactente
Masculino
Paquistão/epidemiologia
Paralisia/virologia
Filogenia
Poliomielite/prevenção & controle
Análise de Sequência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Capsid Proteins); 0 (echovirus 9 capsid protein vp1)
[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:170726
[St] Status:MEDLINE
[do] DOI:10.1017/S0950268817001522


  10 / 4296 MEDLINE  
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[PMID]:28633417
[Au] Autor:Dave P; George B; Sharma DK; Das S
[Ad] Endereço:Department of Microbiology and Cell Biology, Indian Institute of Science, Bangalore 560012, Karnataka, India.
[Ti] Título:Polypyrimidine tract-binding protein (PTB) and PTB-associated splicing factor in CVB3 infection: an ITAF for an ITAF.
[So] Source:Nucleic Acids Res;45(15):9068-9084, 2017 Sep 06.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The 5' UTR of Coxsackievirus B3 (CVB3) contains internal ribosome entry site (IRES), which allows cap-independent translation of the viral RNA and a 5'-terminal cloverleaf structure that regulates viral replication, translation and stability. Here, we demonstrate that host protein PSF (PTB associated splicing factor) interacts with the cloverleaf RNA as well as the IRES element. PSF was found to be an important IRES trans acting factor (ITAF) for efficient translation of CVB3 RNA. Interestingly, cytoplasmic abundance of PSF protein increased during CVB3 infection and this is regulated by phosphorylation status at two different amino acid positions. Further, PSF protein was up-regulated in CVB3 infection. The expression of CVB3-2A protease alone could also induce increased PSF protein levels. Furthermore, we observed the presence of an IRES element in the 5'UTR of PSF mRNA, which is activated during CVB3 infection and might contribute to the elevated levels of PSF. It appears that PSF IRES is also positively regulated by PTB, which is known to regulate CVB3 IRES. Taken together, the results suggest for the first time a novel mechanism of regulations of ITAFs during viral infection, where an ITAF undergoes IRES mediated translation, sustaining its protein levels under condition of translation shut-off.
[Mh] Termos MeSH primário: Enterovirus Humano B/genética
Interações Hospedeiro-Patógeno
Fator de Processamento Associado a PTB/genética
Biossíntese de Proteínas
RNA Viral/genética
Ribossomos/genética
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas
Cisteína Endopeptidases/genética
Cisteína Endopeptidases/metabolismo
Enterovirus Humano B/metabolismo
Regulação da Expressão Gênica
Células HeLa
Seres Humanos
Sítios Internos de Entrada Ribossomal
Conformação de Ácido Nucleico
Fator de Processamento Associado a PTB/antagonistas & inibidores
Fator de Processamento Associado a PTB/metabolismo
Fosforilação
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
RNA Viral/química
RNA Viral/metabolismo
Ribossomos/metabolismo
Transdução de Sinais
Proteínas Virais/genética
Proteínas Virais/metabolismo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (Internal Ribosome Entry Sites); 0 (PTB-Associated Splicing Factor); 0 (RNA, Messenger); 0 (RNA, Small Interfering); 0 (RNA, Viral); 0 (Viral Proteins); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.29 (picornain 2A, Picornavirus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx519



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