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  1 / 30881 MEDLINE  
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[PMID]:29380441
[Au] Autor:Waugh CA; Arukwe A; Jaspers VLB
[Ad] Endereço:Environmental Toxicology, Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
[Ti] Título:Deregulation of microRNA-155 and its transcription factor NF-kB by polychlorinated biphenyls during viral infections.
[So] Source:APMIS;126(3):234-240, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.
[Mh] Termos MeSH primário: Imunidade Inata/genética
MicroRNAs/genética
NF-kappa B/genética
Poli I-C/farmacologia
Bifenilos Policlorados/química
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Embrião de Galinha
Galinhas/genética
Galinhas/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Viroses/genética
Viroses/imunologia
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); DFC2HB4I0K (Polychlorinated Biphenyls); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12811


  2 / 30881 MEDLINE  
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[PMID]:29458688
[Au] Autor:Mitchell SL; Chang YC; Feemster K; Cárdenas AM
[Ad] Endereço:1​Clinical Microbiology Laboratory, Children's Hospital of Pittsburgh of UPMC and Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
[Ti] Título:Implementation of a rapid influenza A/B and RSV direct molecular assay improves emergency department oseltamivir use in paediatric patients.
[So] Source:J Med Microbiol;67(3):358-363, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Influenza A virus (FluA), influenza B virus (FluB) and respiratory syncytial virus (RSV) illnesses increase hospitalizations during seasonal epidemics. METHODOLOGY: To determine the utility of the Simplexa FluA/B & RSV Direct Assay (Direct Flu/RSV) and its impact on oseltamivir use, we offered this assay to emergency department (ED) patients with influenza-like illness. RESULTS: Utilization of the Direct Flu/RSV provided a turnaround time (TAT) of 2 hours. Compared to the flu season prior to implementation of the Direct Flu/RSV, clinicians were more likely to prescribe 5 days of oseltamivir therapy for Direct Flu/RSV-positive patients in comparison to those with a negative test. CONCLUSIONS: Use of Direct Flu/RSV provides results rapidly, which leads to more appropriate use of oseltamivir. The ease of use of this assay and quick TAT allows for prompt decision-making, which is essential for patient care and effective disease control during the influenza season.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Influenza Humana/diagnóstico
Influenza Humana/tratamento farmacológico
Técnicas de Diagnóstico Molecular
Oseltamivir/uso terapêutico
Infecções por Vírus Respiratório Sincicial/diagnóstico
[Mh] Termos MeSH secundário: Antivirais/administração & dosagem
Criança
Saúde da Criança
Pré-Escolar
Serviço Hospitalar de Emergência
Feminino
Seres Humanos
Vírus da Influenza A/genética
Vírus da Influenza A/isolamento & purificação
Vírus da Influenza B/genética
Vírus da Influenza B/isolamento & purificação
Influenza Humana/virologia
Masculino
Nasofaringe/virologia
Oseltamivir/administração & dosagem
Kit de Reagentes para Diagnóstico
Reação em Cadeia da Polimerase em Tempo Real
Infecções por Vírus Respiratório Sincicial/virologia
Vírus Sinciciais Respiratórios/genética
Vírus Sinciciais Respiratórios/isolamento & purificação
Sensibilidade e Especificidade
Resultado do Tratamento
Viroses/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (Reagent Kits, Diagnostic); 20O93L6F9H (Oseltamivir)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180221
[St] Status:MEDLINE
[do] DOI:10.1099/jmm.0.000676


  3 / 30881 MEDLINE  
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[PMID]:29269545
[Ti] Título:Equine disease surveillance: quarterly summary.
[So] Source:Vet Rec;181(25):674-677, 2017 12 23.
[Is] ISSN:2042-7670
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Surtos de Doenças/veterinária
Doenças dos Cavalos/epidemiologia
Vigilância de Evento Sentinela/veterinária
[Mh] Termos MeSH secundário: Animais
Infecções Bacterianas/epidemiologia
Infecções Bacterianas/veterinária
Feminino
Cavalos
Masculino
Doenças Parasitárias em Animais/epidemiologia
Reino Unido/epidemiologia
Viroses/epidemiologia
Viroses/veterinária
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1136/vr.j5900


  4 / 30881 MEDLINE  
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[PMID]:28467275
[Au] Autor:Dos Santos PF; Mansur DS
[Ad] Endereço:Departament of Microbiology, Immunology and Parasitology, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina , Santa Catarina, Brazil .
[Ti] Título:Beyond ISGlylation: Functions of Free Intracellular and Extracellular ISG15.
[So] Source:J Interferon Cytokine Res;37(6):246-253, 2017 Jun.
[Is] ISSN:1557-7465
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ISG15 is a ubiquitin-like type I IFN-stimulated protein of 15 kDa and is one of the most prominently expressed proteins in viral infections. ISG15 is widely known to be involved in a process called ISGylation, where it binds to over 150 targets from a variety of classes of proteins including central immune signaling pathways such as those mediated by NFκB, JNK, and IRF-3. However, ISG15 also exists in a free form that can act intra- or extracellularly. In vitro and in vivo evidences suggest that free ISG15 play different roles in several cellular processes, from cancer and defense against viral infections to activation of immune cells such as lymphocytes, monocytes, and NK cells. This review discusses the roles of free intracellular and secreted ISG15 approaching questions yet to be answered about the mechanism of action of this protein.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Citocinas/imunologia
Interferon gama/imunologia
Transdução de Sinais/imunologia
Ubiquitinas/imunologia
Viroses/imunologia
[Mh] Termos MeSH secundário: Infecções Bacterianas/genética
Infecções Bacterianas/microbiologia
Citocinas/genética
Regulação da Expressão Gênica
Seres Humanos
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Interferon Tipo I/genética
Interferon Tipo I/imunologia
Interferon gama/genética
Monócitos/imunologia
Monócitos/microbiologia
Monócitos/virologia
Neutrófilos/imunologia
Neutrófilos/microbiologia
Neutrófilos/virologia
Linfócitos T/imunologia
Linfócitos T/microbiologia
Linfócitos T/virologia
Ubiquitinas/genética
Viroses/genética
Viroses/virologia
eIF-2 Quinase/genética
eIF-2 Quinase/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cytokines); 0 (IRF3 protein, human); 0 (Interferon Regulatory Factor-3); 0 (Interferon Type I); 0 (Ubiquitins); 60267-61-0 (ISG15 protein, human); 82115-62-6 (Interferon-gamma); EC 2.7.11.1 (eIF-2 Kinase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1089/jir.2016.0103


  5 / 30881 MEDLINE  
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[PMID]:28453680
[Au] Autor:Holtz Y; David JL; Ranwez V
[Ad] Endereço:Montpellier Supagro, Department BE, UMR AGAP, 34060 Montpellier, France.
[Ti] Título:The genetic map comparator: a user-friendly application to display and compare genetic maps.
[So] Source:Bioinformatics;33(9):1387-1388, 2017 05 01.
[Is] ISSN:1367-4811
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Motivation: Marker-assisted selection strongly relies on genetic maps to accelerate breeding programs. High-density maps are now available for numerous species. Dedicated tools are required to compare several high-density maps on the basis of their key characteristics, while pinpointing their differences and similarities. Results: We developed the Genetic Map Comparator-a web-based application for easy comparison of different maps according to their key statistics and the relative positions of common markers. Availability and Implementation: The Genetic Map Comparator is available online at: http://bioweb.supagro.inra.fr/geneticMapComparator. The source code is freely available on GitHub under the under the CeCILL general public license: https://github.com/holtzy/GenMap-Comparator. Contact: Holtz@supagro.fr; Ranwez@supagro.fr.
[Mh] Termos MeSH primário: Genômica/métodos
Análise de Sequência de DNA/métodos
Software
[Mh] Termos MeSH secundário: Resistência à Doença/genética
Genes de Plantas
Doenças das Plantas/genética
Locos de Características Quantitativas
Triticum/genética
Triticum/virologia
Viroses/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/bioinformatics/btw816


  6 / 30881 MEDLINE  
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[PMID]:29293661
[Au] Autor:Monson EA; Crosse KM; Das M; Helbig KJ
[Ad] Endereço:Department of Physiology, Anatomy and Microbiology, La Trobe University, Melbourne, Victoria.
[Ti] Título:Lipid droplet density alters the early innate immune response to viral infection.
[So] Source:PLoS One;13(1):e0190597, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cellular localisation of many innate signalling events following viral infection has yet to be elucidated, however there has been a few cases in which membranes of certain cellular organelles have acted as platforms to these events. Of these, lipid droplets (LDs) have recently been identified as signalling platforms for innate TLR7 and 9 signalling. Despite their wide range of similar roles in various metabolic pathways, LDs have been overlooked as potential platforms for antiviral innate signalling events. This study established an in vitro model to evaluate the efficiency of the early innate immune response in cells with reduced LD content to the viral mimics, dsDNA and dsRNA, and Sendai viral infection. Using RT-qPCR, the expression of IFN-ß and IFN-λ was quantified following stimulation along with the expression of specific ISGs. Luciferase based assays evaluated the combined expression of ISRE-promoter driven ISGs under IFN-ß stimulation. Cellular LD content did not alter the entry of fluorescently labelled viral mimics into cells, but significantly decreased the ability of both Huh-7 and HeLa cells to produce type I and III IFN, as well as downstream ISG expression, indicative of an impeded innate immune response. This observation was also seen during Sendai virus infection of HeLa cells, where both control and LD reduced cells replicated the virus to the same level, but a significantly impaired type I and III IFN response was observed in the LD reduced cells. In addition to altered IFN production, cells with reduced LD content exhibited decreased expression of specific antiviral ISGs: Viperin, IFIT-1 and OAS-1 under IFN-ß stimulation; However the overall induction of the ISRE-promoter was not effected. This study implicates a role for LDs in an efficient early innate host response to viral infection and future work will endeavour to determine the precise role these important organelles play in induction of an antiviral response.
[Mh] Termos MeSH primário: Imunidade Inata
Gotículas Lipídicas/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Western Blotting
Linhagem Celular
Meios de Cultura
Seres Humanos
Interferon Tipo I/imunologia
Ácidos Nucleicos/metabolismo
RNA de Cadeia Dupla/imunologia
Reação em Cadeia da Polimerase em Tempo Real
Vírus Sendai/patogenicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media); 0 (Interferon Type I); 0 (Nucleic Acids); 0 (RNA, Double-Stranded)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180103
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190597


  7 / 30881 MEDLINE  
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[PMID]:28462521
[Au] Autor:Orozco S; Oberst A
[Ad] Endereço:Department of Immunology, University of Washington, Seattle, WA, USA.
[Ti] Título:RIPK3 in cell death and inflammation: the good, the bad, and the ugly.
[So] Source:Immunol Rev;277(1):102-112, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases-1 (RIPK1) and RIPK3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions. Interestingly, accumulating evidence suggests that RIPK3 has functions beyond the induction of necroptotic cell death, especially in the areas of tissue injury and sterile inflammation. Here, we will discuss the role of RIPK3 in a variety of physiological conditions, including necroptotic and non-necroptotic cell death, in the context of viral and bacterial infections, tissue damage, and inflammation.
[Mh] Termos MeSH primário: Infecções Bacterianas/imunologia
Inflamação/imunologia
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Viroses/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Degradação Necrótica do DNA
Seres Humanos
Necrose
Receptores de Morte Celular/metabolismo
Receptores de Reconhecimento de Padrão/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Receptors, Death Domain); 0 (Receptors, Pattern Recognition); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12536


  8 / 30881 MEDLINE  
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[PMID]:28462524
[Au] Autor:Upton JW; Shubina M; Balachandran S
[Ad] Endereço:Department of Molecular Biosciences, LaMontagne Center for Infectious Disease, University of Texas, Austin, TX, USA.
[Ti] Título:RIPK3-driven cell death during virus infections.
[So] Source:Immunol Rev;277(1):90-101, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The programmed self-destruction of infected cells is a powerful antimicrobial strategy in metazoans. For decades, apoptosis represented the dominant mechanism by which the virus-infected cell was thought to undergo programmed cell death. More recently, however, new mechanisms of cell death have been described that are also key to host defense. One such mechanism in vertebrates is programmed necrosis, or "necroptosis", driven by receptor-interacting protein kinase 3 (RIPK3). Once activated by innate immune stimuli, including virus infections, RIPK3 phosphorylates the mixed lineage kinase domain-like protein (MLKL), which then disrupts cellular membranes to effect necroptosis. Emerging evidence demonstrates that RIPK3 can also mediate apoptosis and regulate inflammasomes. Here, we review studies on the mechanisms by which viruses activate RIPK3 and the pathways engaged by RIPK3 that drive cell death.
[Mh] Termos MeSH primário: Inflamassomos/metabolismo
Proteínas Quinases/metabolismo
Proteína Serina-Treonina Quinases de Interação com Receptores/metabolismo
Viroses/imunologia
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Apoptose
Seres Humanos
Imunidade Inata
Necrose
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Inflammasomes); EC 2.7.- (MLKL protein, human); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (RIPK3 protein, human); EC 2.7.11.1 (Receptor-Interacting Protein Serine-Threonine Kinases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12539


  9 / 30881 MEDLINE  
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[PMID]:29111456
[Au] Autor:Smeele ZE; Ainley DG; Varsani A
[Ad] Endereço:The Biodesign Center for Fundamental and Applied Microbiomics, Center for Evolution and Medicine, School of Life Sciences, Arizona State University, Tempe, AZ 85287-5001, USA; School of Biological Sciences, University of Canterbury, Private Bag 4800, Christchurch, New Zealand.
[Ti] Título:Viruses associated with Antarctic wildlife: From serology based detection to identification of genomes using high throughput sequencing.
[So] Source:Virus Res;243:91-105, 2018 01 02.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The Antarctic, sub-Antarctic islands and surrounding sea-ice provide a unique environment for the existence of organisms. Nonetheless, birds and seals of a variety of species inhabit them, particularly during their breeding seasons. Early research on Antarctic wildlife health, using serology-based assays, showed exposure to viruses in the families Birnaviridae, Flaviviridae, Herpesviridae, Orthomyxoviridae and Paramyxoviridae circulating in seals (Phocidae), penguins (Spheniscidae), petrels (Procellariidae) and skuas (Stercorariidae). It is only during the last decade or so that polymerase chain reaction-based assays have been used to characterize viruses associated with Antarctic animals. Furthermore, it is only during the last five years that full/whole genomes of viruses (adenoviruses, anelloviruses, orthomyxoviruses, a papillomavirus, paramyoviruses, polyomaviruses and a togavirus) have been sequenced using Sanger sequencing or high throughput sequencing (HTS) approaches. This review summaries the knowledge of animal Antarctic virology and discusses potential future directions with the advent of HTS in virus discovery and ecology.
[Mh] Termos MeSH primário: Animais Selvagens/virologia
Genoma Viral
Viroses/veterinária
Vírus/isolamento & purificação
[Mh] Termos MeSH secundário: Animais
Animais Selvagens/sangue
Regiões Antárticas
Anticorpos Antivirais/sangue
Sequenciamento de Nucleotídeos em Larga Escala
Viroses/sangue
Viroses/virologia
Vírus/classificação
Vírus/genética
Vírus/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antibodies, Viral)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171108
[St] Status:MEDLINE


  10 / 30881 MEDLINE  
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[PMID]:29210542
[Au] Autor:Nagafuchi S
[Ti] Título:Regulation of Viral Infection and Type 1 Diabetes ; Future Perspective.
[So] Source:Fukuoka Igaku Zasshi;107(6):105-14, 2016 06.
[Is] ISSN:0016-254X
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/complicações
Viroses/complicações
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Linfócitos B/imunologia
Seres Humanos
Viroses/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE



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