Base de dados : MEDLINE
Pesquisa : B04.280.210.400 [Categoria DeCS]
Referências encontradas : 698 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 70 ir para página                         

  1 / 698 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29458559
[Au] Autor:Wada Y; Sasaki M; Setiyono A; Handharyani E; Rahmadani I; Taha S; Adiani S; Latief M; Kholilullah ZA; Subangkit M; Kobayashi S; Nakamura I; Kimura T; Orba Y; Sawa H
[Ad] Endereço:1​Division of Molecular Pathobiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Hokkaido, Japan.
[Ti] Título:Detection of novel gammaherpesviruses from fruit bats in Indonesia.
[So] Source:J Med Microbiol;67(3):415-422, 2018 Mar.
[Is] ISSN:1473-5644
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Bats are an important natural reservoir of zoonotic viral pathogens. We previously isolated an alphaherpesvirus in fruit bats in Indonesia, and here establish the presence of viruses belonging to other taxa of the family Herpesviridae. We screened the same fruit bat population with pan-herpesvirus PCR and discovered 68 sequences of novel gammaherpesvirus, designated 'megabat gammaherpesvirus' (MgGHV). A phylogenetic analysis of approximately 3.4 kbp of continuous MgGHV sequences encompassing the glycoprotein B gene and DNA polymerase gene revealed that the MgGHV sequences are distinct from those of other reported gammaherpesviruses. Further analysis suggested the existence of co-infections of herpesviruses in Indonesian fruit bats. Our findings extend our understanding of the infectious cycles of herpesviruses in bats in Indonesia and the phylogenetic diversity of the gammaherpesviruses.
[Mh] Termos MeSH primário: Quirópteros/virologia
Gammaherpesvirinae/genética
Gammaherpesvirinae/isolamento & purificação
Infecções por Herpesviridae/veterinária
[Mh] Termos MeSH secundário: Animais
Coinfecção/epidemiologia
Coinfecção/veterinária
Coinfecção/virologia
DNA Viral/genética
Reservatórios de Doenças
Gammaherpesvirinae/classificação
Herpesviridae/genética
Herpesviridae/isolamento & purificação
Infecções por Herpesviridae/epidemiologia
Infecções por Herpesviridae/virologia
Seres Humanos
Indonésia/epidemiologia
Filogenia
Reação em Cadeia da Polimerase
Análise de Sequência de DNA
Proteínas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Viral Proteins)
[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.0.000689


  2 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28467282
[Au] Autor:Ferrante JA; Cortés-Hinojosa G; Archer LL; Wellehan JFX
[Ad] Endereço:Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL.
[Ti] Título:Development of a quantitative PCR assay for measurement of trichechid herpesvirus 1 load in the Florida manatee ( Trichechus manatus latirostris).
[So] Source:J Vet Diagn Invest;29(4):476-482, 2017 Jul.
[Is] ISSN:1943-4936
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trichechid herpesvirus 1 (TrHV-1) is currently the only known herpesvirus in any sirenian. We hypothesized that stress may lead to recrudescence of TrHV-1 in manatees, thus making TrHV-1 a potential biomarker of stress. We optimized and validated a TrHV-1 real-time quantitative probe hybridization PCR (qPCR) assay that was used to quantify TrHV-1 in manatee peripheral blood mononuclear cells (PBMCs). Average baseline TrHV-1 loads in a clinically healthy wild Florida manatee ( Trichechus manatus latirostris) population ( n = 42) were 40.9 ± SD 21.2 copies/100 ng DNA; 19 of 42 manatees were positive. TrHV-1 loads were significantly different between the 2 field seasons ( p < 0.025). This optimized and validated qPCR assay may be used as a tool for further research into TrHV-1 in Florida manatees.
[Mh] Termos MeSH primário: Gammaherpesvirinae/isolamento & purificação
Infecções por Herpesviridae/veterinária
Reação em Cadeia da Polimerase em Tempo Real/veterinária
Trichechus manatus
[Mh] Termos MeSH secundário: Animais
Feminino
Florida/epidemiologia
Infecções por Herpesviridae/diagnóstico
Infecções por Herpesviridae/epidemiologia
Masculino
Prevalência
Reação em Cadeia da Polimerase em Tempo Real/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1177/1040638717707554


  3 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29059246
[Au] Autor:Sorel O; Chen T; Myster F; Javaux J; Vanderplasschen A; Dewals BG
[Ad] Endereço:Immunology-Vaccinology, Department of infectious and parasitic diseases, Faculty of Veterinary medicine-FARAH, University of Liège, Liège, Belgium.
[Ti] Título:Macavirus latency-associated protein evades immune detection through regulation of protein synthesis in cis depending upon its glycin/glutamate-rich domain.
[So] Source:PLoS Pathog;13(10):e1006691, 2017 Oct.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alcelaphine herpesvirus 1 (AlHV-1) is a γ-herpesvirus (γ-HV) belonging to the macavirus genus that persistently infects its natural host, the wildebeest, without inducing any clinical sign. However, cross-transmission to other ruminant species causes a deadly lymphoproliferative disease named malignant catarrhal fever (MCF). AlHV-1 ORF73 encodes the latency-associated nuclear antigen (LANA)-homolog protein (aLANA). Recently, aLANA has been shown to be essential for viral persistence in vivo and induction of MCF, suggesting that aLANA shares key properties of other γ-HV genome maintenance proteins. Here we have investigated the evasion of the immune response by aLANA. We found that a glycin/glutamate (GE)-rich repeat domain was sufficient to inhibit in cis the presentation of an epitope linked to aLANA. Although antigen presentation in absence of GE was dependent upon proteasomal degradation of aLANA, a lack of GE did not affect protein turnover. However, protein self-synthesis de novo was downregulated by aLANA GE, a mechanism directly associated with reduced antigen presentation in vitro. Importantly, codon-modification of aLANA GE resulted in increased antigen presentation in vitro and enhanced induction of antigen-specific CD8+ T cell responses in vivo, indicating that mRNA constraints in GE rather than peptidic sequence are responsible for cis-limitation of antigen presentation. Nonetheless, GE-mediated limitation of antigen presentation in cis of aLANA was dispensable during MCF as rabbits developed the disease after virus infection irrespective of the expression of full-length or GE-deficient aLANA. Altogether, we provide evidence that inhibition in cis of protein synthesis through GE is likely involved in long-term immune evasion of AlHV-1 latent persistence in the wildebeest natural host, but dispensable in MCF pathogenesis.
[Mh] Termos MeSH primário: Gammaherpesvirinae/imunologia
Evasão da Resposta Imune/imunologia
Febre Catarral Maligna/imunologia
Proteínas Virais/química
Proteínas Virais/imunologia
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno/imunologia
Bovinos
Ácido Glutâmico/imunologia
Glicina/imunologia
Latência Viral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Proteins); 3KX376GY7L (Glutamic Acid); TE7660XO1C (Glycine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171024
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006691


  4 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28916522
[Au] Autor:Cross SN; Potter JA; Aldo P; Kwon JY; Pitruzzello M; Tong M; Guller S; Rothlin CV; Mor G; Abrahams VM
[Ad] Endereço:Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06510; and.
[Ti] Título:Viral Infection Sensitizes Human Fetal Membranes to Bacterial Lipopolysaccharide by MERTK Inhibition and Inflammasome Activation.
[So] Source:J Immunol;199(8):2885-2895, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chorioamnionitis, premature rupture of fetal membranes (FMs), and subsequent preterm birth are associated with local infection and inflammation, particularly IL-1ß production. Although bacterial infections are commonly identified, other microorganisms may play a role in the pathogenesis. Because viral pandemics, such as influenza, Ebola, and Zika, are becoming more common, and pregnant women are at increased risk for associated complications, this study evaluated the impact that viral infection had on human FM innate immune responses. This study shows that a herpes viral infection of FMs sensitizes the tissue to low levels of bacterial LPS, giving rise to an exaggerated IL-1ß response. Using an ex vivo human FM explant system and an in vivo mouse model of pregnancy, we report that the mechanism by which this aggravated inflammation arises is through the inhibition of the TAM receptor, MERTK, and activation of the inflammasome. The TAM receptor ligand, growth arrest specific 6, re-establishes the normal FM response to LPS by restoring and augmenting TAM receptor and ligand expression, as well as by preventing the exacerbated IL-1ß processing and secretion. These findings indicate a novel mechanism by which viruses alter normal FM immune responses to bacteria, potentially giving rise to adverse pregnancy outcomes.
[Mh] Termos MeSH primário: Membranas Extraembrionárias/imunologia
Gammaherpesvirinae/imunologia
Infecções por Herpesviridae/imunologia
Herpesvirus Humano 2/imunologia
Inflamassomos/metabolismo
Nascimento Prematuro/imunologia
Proteínas Proto-Oncogênicas/metabolismo
Receptores Proteína Tirosina Quinases/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Corioamnionite
Feminino
Infecções por Herpesviridae/complicações
Seres Humanos
Imunização
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Interleucina-1beta/metabolismo
Lipopolissacarídeos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Gravidez
Nascimento Prematuro/etiologia
Proteínas Proto-Oncogênicas/genética
Receptores Proteína Tirosina Quinases/genética
c-Mer Tirosina Quinase
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammasomes); 0 (Intercellular Signaling Peptides and Proteins); 0 (Interleukin-1beta); 0 (Lipopolysaccharides); 0 (Proto-Oncogene Proteins); 0 (growth arrest-specific protein 6); EC 2.7.10.1 (MERTK protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (c-Mer Tyrosine Kinase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170917
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700870


  5 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28105852
[Au] Autor:Janícková O; Ancicová L; Briestenská K; Mistríková J
[Ti] Título:The effect of Isoprinosine treatment on persistent infection of Balb/c mice infected with murine gammaherpesvirus 68.
[So] Source:Acta Virol;61(1):32-38, 2017.
[Is] ISSN:0001-723X
[Cp] País de publicação:Slovakia
[La] Idioma:eng
[Ab] Resumo:We demonstrated the positive effect of Isoprinosine treatment on persistent infection of Balb/c mice with murine gammaherpesvirus 68 (MHV-68). Increased number of leukocytes, increased percentage of neutrophils, elevated levels of virus-neutralizing (VN) antibodies, reduced number of atypical lymphocytes and reduced virus titers were detected in the examined organs after a 14-day treatment. The positive effect of Isoprinosine therapy vanished after 120-150 days. After this interval, we demonstrated lower numbers of leukocytes, lower levels of VN antibodies and an increased number of atypical lymphoid monocytes in the Isoprinosine-treated group. Immunological parameters correlated with increased titers of virus in all investigated organs. Evidence of immunostimulation was demonstrated by lower incidence of tumor formation (7.5%) in the group of MHV-infected and Isoprinosine-treated mice in comparison to group without Isoprinosine treatment (17.5%). The presented results showed that Isoprinosine therapy had a positive impact on persistent infection of mice with MHV-68, but this effect was time-limited. The improvement of the investigated parameters lasted for five months only. Our presented results confirmed that each treatment with Isoprinosine should be repeated and must be long-term in some chronic infections.
[Mh] Termos MeSH primário: Antivirais/uso terapêutico
Gammaherpesvirinae
Infecções por Herpesviridae/tratamento farmacológico
Inosina Pranobex/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Cercopithecus aethiops
Macrófagos Peritoneais/virologia
Camundongos
Camundongos Endogâmicos BALB C
Células NIH 3T3
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiviral Agents); W1SO0V223F (Inosine Pranobex)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.4149/av_2017_01_32


  6 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28069010
[Au] Autor:Sattler C; Moritz F; Chen S; Steer B; Kutschke D; Irmler M; Beckers J; Eickelberg O; Schmitt-Kopplin P; Adler H; Stoeger T
[Ad] Endereço:Helmholtz Zentrum München - German Research Center for Environmental Health (GmbH), Comprehensive Pneumology Center, Institute of Lung Biology and Disease, Ingolstädter Landstr. 1, D-85764, Neuherberg, Germany.
[Ti] Título:Nanoparticle exposure reactivates latent herpesvirus and restores a signature of acute infection.
[So] Source:Part Fibre Toxicol;14(1):2, 2017 01 10.
[Is] ISSN:1743-8977
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Inhalation of environmental (nano) particles (NP) as well as persistent herpesvirus-infection are potentially associated with chronic lung disease and as both are omnipresent in human society a coincidence of these two factors is highly likely. We hypothesized that NP-exposure of persistently herpesvirus-infected cells as a second hit might disrupt immune control of viral latency, provoke reactivation of latent virus and eventually lead to an inflammatory response and tissue damage. RESULTS: To test this hypothesis, we applied different NP to cells or mice latently infected with murine gammaherpesvirus 68 (MHV-68) which provides a small animal model for the study of gammaherpesvirus-pathogenesis in vitro and in vivo. In vitro, NP-exposure induced expression of the typically lytic viral gene ORF50 and production of lytic virus. In vivo, lytic viral proteins in the lung increased after intratracheal instillation with NP and elevated expression of the viral gene ORF50 could be detected in cells from bronchoalveolar lavage. Gene expression and metabolome analysis of whole lung tissue revealed patterns with striking similarities to acute infection. Likewise, NP-exposure of human cells latently infected with Epstein-Barr-Virus also induced virus production. CONCLUSIONS: Our results indicate that NP-exposure of persistently herpesvirus-infected cells - murine or human - restores molecular signatures found in acute virus infection, boosts production of lytic viral proteins, and induces an inflammatory response in the lung - a combination which might finally result in tissue damage and pathological alterations.
[Mh] Termos MeSH primário: Gammaherpesvirinae/efeitos dos fármacos
Infecções por Herpesviridae/virologia
Nanopartículas/toxicidade
Ativação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Cricetinae
Gammaherpesvirinae/fisiologia
Camundongos
Células NIH 3T3
Latência Viral
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170317
[Lr] Data última revisão:
170317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1186/s12989-016-0181-1


  7 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28053110
[Au] Autor:AlHajri SM; Cunha CW; Nicola AV; Aguilar HC; Li H; Taus NS
[Ad] Endereço:Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, Washington, USA.
[Ti] Título:Ovine Herpesvirus 2 Glycoproteins B, H, and L Are Sufficient for, and Viral Glycoprotein Ov8 Can Enhance, Cell-Cell Membrane Fusion.
[So] Source:J Virol;91(6), 2017 Mar 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ovine herpesvirus 2 (OvHV-2) is a gammaherpesvirus in the genus that is carried asymptomatically by sheep. Infection of poorly adapted animals with OvHV-2 results in sheep-associated malignant catarrhal fever, a fatal disease characterized by lymphoproliferation and vasculitis. There is no treatment or vaccine for the disease and no cell culture system to propagate the virus. The lack of cell culture has hindered studies of OvHV-2 biology, including its entry mechanism. As an alternative method to study OvHV-2 glycoproteins responsible for membrane fusion as a part of the entry mechanism, we developed a virus-free cell-to-cell membrane fusion assay to identify the minimum required OvHV-2 glycoproteins to induce membrane fusion. OvHV-2 glycoproteins B, H, and L (gB, gH, and gL) were able to induce membrane fusion together but not when expressed individually. Additionally, open reading frame Ov8, unique to OvHV-2, was found to encode a transmembrane glycoprotein that can significantly enhance membrane fusion. Thus, OvHV-2 gB, gH, and gL are sufficient to induce membrane fusion, while glycoprotein Ov8 plays an enhancing role by an unknown mechanism. Herpesviruses enter cells via attachment of the virion to the cellular surface and fusion of the viral envelope with cellular membranes. Virus-cell membrane fusion is an important step for a successful viral infection. Elucidating the roles of viral glycoproteins responsible for membrane fusion is critical toward understanding viral entry. Entry of ovine herpesvirus 2 (OvHV-2), the causative agent of sheep associated-malignant catarrhal fever, which is one of the leading causes of death in bison and other ungulates, has not been well studied due to the lack of a cell culture system to propagate the virus. The identification of OvHV-2 glycoproteins that mediate membrane fusion may help identify viral and/or cellular factors involved in OvHV-2 cell tropism and will advance investigation of cellular factors necessary for virus-cell membrane fusion. We found that OvHV-2 glycoproteins B, H, and L are sufficient for, and viral glycoprotein Ov8 can significantly enhance, cell-cell membrane fusion.
[Mh] Termos MeSH primário: Fusão Celular
Gammaherpesvirinae/fisiologia
Interações Hospedeiro-Patógeno
Proteínas Estruturais Virais/metabolismo
Internalização do Vírus
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Viral Structural Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE


  8 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27902371
[Au] Autor:Mekuria ZH; El-Hage C; Ficorilli NP; Washington EA; Gilkerson JR; Hartley CA
[Ad] Endereço:1​Faculty of Veterinary and Agricultural Science, The University of Melbourne, VIC 3010, Australia 2​Department of Veterinary Science, Maxwell H. Gluck Equine Research Centre, University of Kentucky, Lexington, KY 40546-0099, USA.
[Ti] Título:Mapping B lymphocytes as major reservoirs of naturally occurring latent equine herpesvirus 5 infection.
[So] Source:J Gen Virol;98(3):461-470, 2017 Mar.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Equine herpesvirus 5 (EHV5) is a commonly detected gammaherpesvirus, which, along with the closely related EHV2, constitute the only two known percaviruses that infect horses. Apart from detection in horse populations worldwide and the recent publication of the whole genome, there is little known about the biology and pathogenesis of this virus, with many assumptions made by parallels with EHV2. The long-term survival of gammaherpesviruses within infected hosts involves the establishment and maintenance of latency in selected cell and tissues types, particularly lymphocytes. A latent gammaherpesvirus infection is characterized by a limited number of genes expressing in a particular cell or tissue type. In this study, we have used in vitro co-culturing to detect EHV5 in equine PBMCs and characterize the predominant cellular site for the establishment and maintenance of a latent infection. These experiments were conducted by isolating PBMCs from 10 horses and sorting subpopulations into two T lymphocyte (CD4 and CD8), B lymphocyte and macrophage enriched or depleted fractions. These lymphocyte and macrophage fractions were examined for the presence of latent EHV5 by in vitro co-culturing with equine foetal kidney cells. The lymphocyte fraction enriched with B lymphocytes had a significantly increased (P=0.005) number of plaques formed during co-culturing, whereas the B lymphocyte depleted fraction had a significant reduction in the number of plaques formed after co-culturing. Taken together, these results demonstrate that equine gammaherpesviruses establish latency in the equine PBMCs, with the predominant site for maintenance of latent virus being B lymphocytes.
[Mh] Termos MeSH primário: Linfócitos B/virologia
Gammaherpesvirinae/fisiologia
Infecções por Herpesviridae/veterinária
Infecções por Herpesviridae/virologia
Doenças dos Cavalos/virologia
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/virologia
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/virologia
Técnicas de Cocultura
Citometria de Fluxo
Gammaherpesvirinae/genética
Gammaherpesvirinae/isolamento & purificação
Genoma Viral
Infecções por Herpesviridae/imunologia
Doenças dos Cavalos/imunologia
Cavalos
Ativação Linfocitária
Macrófagos/imunologia
Macrófagos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161201
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000668


  9 / 698 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27795415
[Au] Autor:Mboko WP; Rekow MM; Ledwith MP; Lange PT; Schmitz KE; Anderson S; Tarakanova VL
[Ad] Endereço:Microbiology and Molecular Genetics, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
[Ti] Título:Interferon Regulatory Factor 1 and Type I Interferon Cooperate To Control Acute Gammaherpesvirus Infection.
[So] Source:J Virol;91(1), 2017 Jan 01.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gammaherpesviruses are ubiquitous pathogens that establish lifelong infection in >95% of adults worldwide and are associated with a variety of malignancies. Coevolution of gammaherpesviruses with their hosts has resulted in an intricate relationship between the virus and the host immune system, and perturbation of the virus-host balance results in pathology. Interferon regulatory factor 1 (IRF-1) is a tumor suppressor that is also involved in the regulation of innate and adaptive immune responses. Here, we show that type I interferon (IFN) and IRF-1 cooperate to control acute gammaherpesvirus infection. Specifically, we demonstrate that a combination of IRF-1 and type I IFN signaling ensures host survival during acute gammaherpesvirus infection and supports IFN gamma-mediated suppression of viral replication. Thus, our studies reveal an intriguing cross talk between IRF-1 and type I and II IFNs in the induction of the antiviral state during acute gammaherpesvirus infection. IMPORTANCE: Gammaherpesviruses establish chronic infection in a majority of adults, and this long-term infection is associated with virus-driven development of a range of malignancies. In contrast, a brief period of active gammaherpesvirus replication during acute infection of a naive host is subclinical in most individuals. Here, we discovered that a combination of type I interferon (IFN) signaling and interferon regulatory factor 1 (IRF-1) expression is required to ensure survival of a gammaherpesvirus-infected host past the first 8 days of infection. Specifically, both type I IFN receptor and IRF-1 expression potentiated antiviral effects of type II IFN to restrict gammaherpesvirus replication in vivo, in the lungs, and in vitro, in primary macrophage cultures.
[Mh] Termos MeSH primário: Gammaherpesvirinae/patogenicidade
Infecções por Herpesviridae/imunologia
Interações Hospedeiro-Patógeno
Fator Regulador 1 de Interferon/genética
Interferon-alfa/genética
Interferon beta/genética
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação Mielomonocítica/genética
Antígenos de Diferenciação Mielomonocítica/imunologia
Antígenos Nucleares/genética
Antígenos Nucleares/imunologia
Gammaherpesvirinae/crescimento & desenvolvimento
Regulação da Expressão Gênica
Infecções por Herpesviridae/genética
Infecções por Herpesviridae/mortalidade
Infecções por Herpesviridae/virologia
Seres Humanos
Fator Regulador 1 de Interferon/imunologia
Fator Regulador 3 de Interferon/genética
Fator Regulador 3 de Interferon/imunologia
Fator Regulador 7 de Interferon/genética
Fator Regulador 7 de Interferon/imunologia
Helicase IFIH1 Induzida por Interferon/genética
Helicase IFIH1 Induzida por Interferon/imunologia
Interferon-alfa/imunologia
Interferon beta/imunologia
Interferon gama/genética
Interferon gama/imunologia
Pulmão/imunologia
Pulmão/virologia
Macrófagos/imunologia
Macrófagos/virologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Cultura Primária de Células
Proteínas/genética
Proteínas/imunologia
Receptor de Interferon alfa e beta/genética
Receptor de Interferon alfa e beta/imunologia
Transdução de Sinais
Baço/imunologia
Baço/virologia
Análise de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, Myelomonocytic); 0 (Antigens, Nuclear); 0 (Ifnar1 protein, mouse); 0 (Interferon Regulatory Factor-1); 0 (Interferon Regulatory Factor-3); 0 (Interferon Regulatory Factor-7); 0 (Interferon-alpha); 0 (Mnda protein, mouse); 0 (Proteins); 0 (vig1 protein, mouse); 156986-95-7 (Receptor, Interferon alpha-beta); 77238-31-4 (Interferon-beta); 82115-62-6 (Interferon-gamma); EC 3.6.1.- (Ifih1 protein, mouse); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161101
[St] Status:MEDLINE


  10 / 698 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:28304247
[Au] Autor:Trammell RA; Toth LA
[Ad] Endereço:Departments of Internal Medicine, Southern Illinois University School of Medicine, Springfield, Illinois.
[Ti] Título:Effects of Chronic Diurnal Disruption and Acute Inflammatory Challenge on Mice with Latent Murine Gammaherpesvirus Infection.
[So] Source:Comp Med;66(6):445-454, 2016 Dec 01.
[Is] ISSN:1532-0820
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:People who engage in shift work (SW) have increased risk of developing illnesses, including infectious diseases and various inflammatory conditions. We hypothesized that exposure to repeated cycles of diurnal disruption, mimicking SW, influences viral clearance, latent viral load, or viral reactivation from latency in mice infected with murine gammaherpesvirus (MuGHV). To test this idea, we inoculated BALB/cByJ and C.129S7(B6)-Ifng tm1Ts/J (IFNgKO) mice with MuGHV and housed them under either a stable light:dark (LD) cycle or one mimicking SW. Compared with BALB/cByJ mice, IFNgKO mice generally had higher levels of lytic virus during the 6-wk period after inoculation. In addition, more IFNgKO mice were positive for replicating virus than were BALB/cByJ mice. Exposure to SW did not alter these measures consistently. After the virus had entered the latent phase of infection, mice received either LPS or pyrogen-free saline intraperitoneally. Mice exposed to SW and then injected with LPS during latent infection had greater viral loads and more replicating virus in the lung at 7 d after injection than did either mice that received pyrogen-free saline or those exposed to LD and then treated with LPS. Some cytokine and chemokine concentrations were changed in lung collected 1 d after but not at 7 d after LPS administration. These findings suggest that exposure to repeated chronic diurnal disruption and an acute inflammatory challenge during latent MuGHV infection, in the context of impaired host immune competence, contribute to enhanced viral reactivity and an increased viral load that might trigger 'sickness behavior' symptoms of infectious disease and perhaps contribute to chronic fatigue syndrome.
[Mh] Termos MeSH primário: Ritmo Circadiano/fisiologia
Doenças Transmissíveis/complicações
Infecções por Herpesviridae/complicações
Carga Viral/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Gammaherpesvirinae
Seres Humanos
Pulmão/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Fotoperíodo
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE



página 1 de 70 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde