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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

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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

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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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