Base de dados : MEDLINE
Pesquisa : B04.820.650.589.650 [Categoria DeCS]
Referências encontradas : 91 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 10 ir para página                        

  1 / 91 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28075409
[Au] Autor:González ME
[Ad] Endereço:Unidad de Expresión Viral, Centro Nacional de Microbiología, Instituto de Salud Carlos III, Carretera de Majadahonda-Pozuelo Km 2, Majadahonda, 28220 Madrid, Spain. megonzalez@isciii.es.
[Ti] Título:The HIV-1 Vpr Protein: A Multifaceted Target for Therapeutic Intervention.
[So] Source:Int J Mol Sci;18(1), 2017 Jan 10.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The human immunodeficiency virus type 1 (HIV-1) Vpr protein is an attractive target for antiretroviral drug development. The conservation both of the structure along virus evolution and the amino acid sequence in viral isolates from patients underlines the importance of Vpr for the establishment and progression of HIV-1 disease. While its contribution to virus replication in dividing and non-dividing cells and to the pathogenesis of HIV-1 in many different cell types, both extracellular and intracellular forms, have been extensively studied, its precise mechanism of action nevertheless remains enigmatic. The present review discusses how the apparently multifaceted interplay between Vpr and host cells may be due to the impairment of basic metabolic pathways. Vpr protein modifies host cell energy metabolism, oxidative status, and proteasome function, all of which are likely conditioned by the concentration and multimerization of the protein. The characterization of Vpr domains along with new laboratory tools for the assessment of their function has become increasingly relevant in recent years. With these advances, it is conceivable that drug discovery efforts involving Vpr-targeted antiretrovirals will experience substantial growth in the coming years.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/farmacologia
Infecções por HIV/etiologia
HIV-1/efeitos dos fármacos
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Fármacos Anti-HIV/uso terapêutico
Proteínas de Transporte/metabolismo
Sequência Conservada
Progressão da Doença
Descoberta de Drogas
Evolução Molecular
Infecções por HIV/tratamento farmacológico
Infecções por HIV/metabolismo
HIV-1/fisiologia
Seres Humanos
Lentivirus de Primatas/genética
Ligação Proteica
Replicação Viral
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/química
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-HIV Agents); 0 (Carrier Proteins); 0 (vpr Gene Products, Human Immunodeficiency Virus); 0 (vpr protein, Human immunodeficiency virus 1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE


  2 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27789390
[Au] Autor:Foley BT; Leitner T; Paraskevis D; Peeters M
[Ad] Endereço:Theoretical Biology and Biophysics Group, T-6 Mail Stop K710, Los Alamos National Laboratory, Los Alamos, NM 87545, USA. Electronic address: btf@lanl.gov.
[Ti] Título:Primate immunodeficiency virus classification and nomenclature: Review.
[So] Source:Infect Genet Evol;46:150-158, 2016 Dec.
[Is] ISSN:1567-7257
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The International Committee for the Taxonomy and Nomenclature of Viruses does not rule on virus classifications below the species level. The definition of species for viruses cannot be clearly defined for all types of viruses. The complex and interesting epidemiology of Human Immunodeficiency Viruses demands a detailed and informative nomenclature system, while at the same time it presents challenges such that many of the rules need to be flexibly applied or modified over time. This review outlines the nomenclature system for primate lentiviruses and provides an update on new findings since the last review was written in 2000.
[Mh] Termos MeSH primário: Infecções por Lentivirus/virologia
Lentivirus de Primatas/classificação
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Filogenia
Primatas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


  3 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26360709
[Au] Autor:Greenwood EJ; Schmidt F; Kondova I; Niphuis H; Hodara VL; Clissold L; McLay K; Guerra B; Redrobe S; Giavedoni LD; Lanford RE; Murthy KK; Rouet F; Heeney JL
[Ad] Endereço:Department of Veterinary Medicine, University of Cambridge, Cambridge, United Kingdom.
[Ti] Título:Simian Immunodeficiency Virus Infection of Chimpanzees (Pan troglodytes) Shares Features of Both Pathogenic and Non-pathogenic Lentiviral Infections.
[So] Source:PLoS Pathog;11(9):e1005146, 2015 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The virus-host relationship in simian immunodeficiency virus (SIV) infected chimpanzees is thought to be different from that found in other SIV infected African primates. However, studies of captive SIVcpz infected chimpanzees are limited. Previously, the natural SIVcpz infection of one chimpanzee, and the experimental infection of six chimpanzees was reported, with limited follow-up. Here, we present a long-term study of these seven animals, with a retrospective re-examination of the early stages of infection. The only clinical signs consistent with AIDS or AIDS associated disease was thrombocytopenia in two cases, associated with the development of anti-platelet antibodies. However, compared to uninfected and HIV-1 infected animals, SIVcpz infected animals had significantly lower levels of peripheral blood CD4+ T-cells. Despite this, levels of T-cell activation in chronic infection were not significantly elevated. In addition, while plasma levels of ß2 microglobulin, neopterin and soluble TNF-related apoptosis inducing ligand (sTRAIL) were elevated in acute infection, these markers returned to near-normal levels in chronic infection, reminiscent of immune activation patterns in 'natural host' species. Furthermore, plasma soluble CD14 was not elevated in chronic infection. However, examination of the secondary lymphoid environment revealed persistent changes to the lymphoid structure, including follicular hyperplasia in SIVcpz infected animals. In addition, both SIV and HIV-1 infected chimpanzees showed increased levels of deposition of collagen and increased levels of Mx1 expression in the T-cell zones of the lymph node. The outcome of SIVcpz infection of captive chimpanzees therefore shares features of both non-pathogenic and pathogenic lentivirus infections.
[Mh] Termos MeSH primário: Doenças dos Símios Antropoides/virologia
HIV-1/fisiologia
Infecções por Lentivirus/veterinária
Lentivirus de Primatas/fisiologia
Pan troglodytes
Síndrome de Imunodeficiência Adquirida dos Símios/virologia
Vírus da Imunodeficiência Símia/fisiologia
[Mh] Termos MeSH secundário: Animais
Doenças dos Símios Antropoides/imunologia
Doenças dos Símios Antropoides/patologia
Doenças dos Símios Antropoides/fisiopatologia
Doenças Autoimunes/etiologia
Doenças Autoimunes/veterinária
Biomarcadores/sangue
Contagem de Linfócito CD4
Feminino
HIV-1/imunologia
HIV-1/isolamento & purificação
Hiperplasia
Infecções por Lentivirus/imunologia
Infecções por Lentivirus/fisiopatologia
Infecções por Lentivirus/virologia
Lentivirus de Primatas/imunologia
Lentivirus de Primatas/isolamento & purificação
Linfonodos/imunologia
Linfonodos/metabolismo
Linfonodos/patologia
Linfonodos/virologia
Masculino
Proteínas de Resistência a Myxovirus/metabolismo
Neopterina/sangue
Fragmentos de Peptídeos/sangue
Fragmentos de Peptídeos/química
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/sangue
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/química
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
Síndrome de Imunodeficiência Adquirida dos Símios/patologia
Síndrome de Imunodeficiência Adquirida dos Símios/fisiopatologia
Vírus da Imunodeficiência Símia/imunologia
Vírus da Imunodeficiência Símia/isolamento & purificação
Trombocitopenia/etiologia
Trombocitopenia/veterinária
Carga Viral
Microglobulina-2 beta/sangue
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Myxovirus Resistance Proteins); 0 (Peptide Fragments); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (beta 2-Microglobulin); 670-65-5 (Neopterin)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170118
[Lr] Data última revisão:
170118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150912
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1005146


  4 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26291613
[Au] Autor:McCarthy KR; Kirmaier A; Autissier P; Johnson WE
[Ad] Endereço:Harvard Program in Virology, Harvard Medical School, Boston, Massachusetts, United States of America; Biology Department, Boston College, Chestnut Hill, Massachusetts, United States of America.
[Ti] Título:Evolutionary and Functional Analysis of Old World Primate TRIM5 Reveals the Ancient Emergence of Primate Lentiviruses and Convergent Evolution Targeting a Conserved Capsid Interface.
[So] Source:PLoS Pathog;11(8):e1005085, 2015 Aug.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The widespread distribution of lentiviruses among African primates, and the lack of severe pathogenesis in many of these natural reservoirs, are taken as evidence for long-term co-evolution between the simian immunodeficiency viruses (SIVs) and their primate hosts. Evidence for positive selection acting on antiviral restriction factors is consistent with virus-host interactions spanning millions of years of primate evolution. However, many restriction mechanisms are not virus-specific, and selection cannot be unambiguously attributed to any one type of virus. We hypothesized that the restriction factor TRIM5, because of its unique specificity for retrovirus capsids, should accumulate adaptive changes in a virus-specific fashion, and therefore, that phylogenetic reconstruction of TRIM5 evolution in African primates should reveal selection by lentiviruses closely related to modern SIVs. We analyzed complete TRIM5 coding sequences of 22 Old World primates and identified a tightly-spaced cluster of branch-specific adaptions appearing in the Cercopithecinae lineage after divergence from the Colobinae around 16 million years ago. Functional assays of both extant TRIM5 orthologs and reconstructed ancestral TRIM5 proteins revealed that this cluster of adaptations in TRIM5 specifically resulted in the ability to restrict Cercopithecine lentiviruses, but had no effect (positive or negative) on restriction of other retroviruses, including lentiviruses of non-Cercopithecine primates. The correlation between lineage-specific adaptations and ability to restrict viruses endemic to the same hosts supports the hypothesis that lentiviruses closely related to modern SIVs were present in Africa and infecting the ancestors of Cercopithecine primates as far back as 16 million years ago, and provides insight into the evolution of TRIM5 specificity.
[Mh] Termos MeSH primário: Proteínas de Transporte/genética
Evolução Molecular
Infecções por Lentivirus/genética
Lentivirus de Primatas
Doenças dos Macacos/genética
Doenças dos Macacos/virologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Western Blotting
Cercopithecidae
Lentivirus
Dados de Sequência Molecular
Filogenia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Carrier Proteins)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150821
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1005085


  5 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26041873
[Au] Autor:Nakano Y; Matsuda K; Yoshikawa R; Yamada E; Misawa N; Hirsch VM; Koyanagi Y; Sato K
[Ad] Endereço:1​Laboratory of Viral Pathogenesis, Institute for Virus Research, Kyoto University, Kyoto 6068507, Japan 2​Department of Medical Virology, Faculty of Life Sciences, Kumamoto University, Kumamoto 8608556, Japan.
[Ti] Título:Down-modulation of primate lentiviral receptors by Nef proteins of simian immunodeficiency virus (SIV) of chimpanzees (SIVcpz) and related SIVs: implication for the evolutionary event at the emergence of SIVcpz.
[So] Source:J Gen Virol;96(9):2867-77, 2015 Sep.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It has been estimated that human immunodeficiency virus type 1 originated from the zoonotic transmission of simian immunodeficiency virus (SIV) of chimpanzees, SIVcpz, and that SIVcpz emerged by the recombination of two lineages of SIVs in Old World monkeys (SIVgsn/mon/mus in guenons and SIVrcm in red-capped mangabeys) and SIVcpz Nef is most closely related to SIVrcm Nef. These observations suggest that SIVrcm Nef had an advantage over SIVgsn/mon/mus during the evolution of SIVcpz in chimpanzees, although this advantage remains uncertain. Nef is a multifunctional protein which downregulates CD4 and coreceptor proteins from the surface of infected cells, presumably to limit superinfection. To assess the possibility that SIVrcm Nef was selected by its superior ability to downregulate viral entry receptors in chimpanzees, we compared its ability to down-modulate viral receptor proteins from humans, chimpanzees and red-capped mangabeys with Nef proteins from eight other different strains of SIVs. Surprisingly, the ability of SIVrcm Nef to downregulate CCR5, CCR2B and CXCR6 was comparable to or lower than SIVgsn/mon/mus Nef, indicating that ability to down-modulate chemokine receptors was not the selective pressure. However, SIVrcm Nef significantly downregulates chimpanzee CD4 over SIVgsn/mon/mus Nefs. Our findings suggest the possibility that the selection of SIVrcm Nef by ancestral SIVcpz is due to its superior capacity to down-modulate chimpanzees CD4 rather than coreceptor proteins.
[Mh] Termos MeSH primário: Evolução Molecular
Produtos do Gene nef/genética
Lentivirus de Primatas/genética
Doenças dos Primatas/genética
Receptores Virais/genética
Síndrome de Imunodeficiência Adquirida dos Símios/genética
Vírus da Imunodeficiência Símia/genética
[Mh] Termos MeSH secundário: Animais
Cercocebus
Produtos do Gene nef/metabolismo
Interações Hospedeiro-Patógeno
Seres Humanos
Lentivirus de Primatas/classificação
Lentivirus de Primatas/metabolismo
Pan troglodytes
Filogenia
Doenças dos Primatas/metabolismo
Doenças dos Primatas/virologia
Primatas
Receptores Virais/metabolismo
Síndrome de Imunodeficiência Adquirida dos Símios/metabolismo
Síndrome de Imunodeficiência Adquirida dos Símios/virologia
Vírus da Imunodeficiência Símia/classificação
Vírus da Imunodeficiência Símia/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gene Products, nef); 0 (Receptors, Virus)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:160901
[Lr] Data última revisão:
160901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150605
[St] Status:MEDLINE
[do] DOI:10.1099/vir.0.000207


  6 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25880110
[Au] Autor:Madison MN; Jones PH; Okeoma CM
[Ad] Endereço:Department of Microbiology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242-1109, USA.
[Ti] Título:Exosomes in human semen restrict HIV-1 transmission by vaginal cells and block intravaginal replication of LP-BM5 murine AIDS virus complex.
[So] Source:Virology;482:189-201, 2015 Aug.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exosomes are membranous extracellular nanovesicles secreted by diverse cell types. Exosomes from healthy human semen have been shown to inhibit HIV-1 replication and to impair progeny virus infectivity. In this study, we examined the ability of healthy human semen exosomes to restrict HIV-1 and LP-BM5 murine AIDS virus transmission in three different model systems. We show that vaginal cells internalize exosomes with concomitant transfer of functional mRNA. Semen exosomes blocked the spread of HIV-1 from vaginal epithelial cells to target cells in our cell-to-cell infection model and suppressed transmission of HIV-1 across the vaginal epithelial barrier in our trans-well model. Our in vivo model shows that human semen exosomes restrict intravaginal transmission and propagation of murine AIDS virus. Our study highlights an antiretroviral role for semen exosomes that may be harnessed for the development of novel therapeutic strategies to combat HIV-1 transmission.
[Mh] Termos MeSH primário: Exossomos/imunologia
Lentivirus de Primatas/imunologia
Lentivirus de Primatas/fisiologia
Sêmen/imunologia
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150417
[St] Status:MEDLINE


  7 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25872908
[Au] Autor:Bächle SM; Sauter D; Sibitz S; Sandberg JK; Kirchhoff F; Moll M
[Ad] Endereço:Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, 14186 Stockholm, Sweden.
[Ti] Título:Involvement of a C-terminal motif in the interference of primate lentiviral Vpu proteins with CD1d-mediated antigen presentation.
[So] Source:Sci Rep;5:9675, 2015 Apr 15.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The HIV-1 accessory protein Vpu is emerging as a critical factor for viral evasion from innate immunity. We have previously shown that the Vpu proteins of two HIV-1 group M subtype B strains (NL4-3 and BaL) down-regulate CD1d from the surface of infected dendritic cells (DCs) and inhibit their crosstalk with the innate invariant natural killer T (iNKT) cells. In the present study, we have investigated the ability of a comprehensive set of primate lentiviral Vpu proteins to interfere with CD1d-mediated immunity. We found that CD1d down-regulation is a conserved function of Vpu proteins from HIV-1 groups M, O and P as well as their direct precursors SIVcpzPtt and SIVgor. At the group M subtype level, subtype C Vpu proteins were significantly weaker CD1d antagonists than subtype B Vpu proteins. Functional characterization of different mutants and chimeras derived from active subtype B and inactive subtype C Vpu proteins revealed that residues in the cytoplasmic domain are important for CD1d down-regulation. Specifically, we identified a C-terminal APW motif characteristic for group M subtype B Vpu proteins necessary for interference with CD1d surface expression. These findings support the notion that Vpu plays an important role in lentiviral evasion from innate immunity.
[Mh] Termos MeSH primário: Apresentação do Antígeno/imunologia
Antígenos CD1d/metabolismo
Lentivirus de Primatas/imunologia
Lentivirus de Primatas/metabolismo
Domínios e Motivos de Interação entre Proteínas
Proteínas Virais Reguladoras e Acessórias/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Animais
Linhagem Celular
Sequência Conservada
Regulação para Baixo
Expressão Gênica
HIV-1/genética
HIV-1/metabolismo
Proteínas do Vírus da Imunodeficiência Humana/química
Proteínas do Vírus da Imunodeficiência Humana/genética
Proteínas do Vírus da Imunodeficiência Humana/metabolismo
Seres Humanos
Lentivirus de Primatas/genética
Ativação Linfocitária/imunologia
Dados de Sequência Molecular
Mutação
Células T Matadoras Naturais/imunologia
Células T Matadoras Naturais/metabolismo
Matrizes de Pontuação de Posição Específica
Proteínas Virais Reguladoras e Acessórias/química
Proteínas Virais Reguladoras e Acessórias/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (Human Immunodeficiency Virus Proteins); 0 (Viral Regulatory and Accessory Proteins); 0 (vpu protein, Human immunodeficiency virus 1)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150416
[St] Status:MEDLINE
[do] DOI:10.1038/srep09675


  8 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25858157
[Au] Autor:Francica JR; Sheng Z; Zhang Z; Nishimura Y; Shingai M; Ramesh A; Keele BF; Schmidt SD; Flynn BJ; Darko S; Lynch RM; Yamamoto T; Matus-Nicodemos R; Wolinsky D; Nason M; Valiante NM; Malyala P; De Gregorio E; Barnett SW; Singh M; O'Hagan DT; Koup RA; Mascola JR; Martin MA; Kepler TB; Douek DC; Shapiro L; Seder RA; NISC Comparative Sequencing Program
[Ad] Endereço:Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
[Ti] Título:Analysis of immunoglobulin transcripts and hypermutation following SHIV(AD8) infection and protein-plus-adjuvant immunization.
[So] Source:Nat Commun;6:6565, 2015 Apr 10.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Developing predictive animal models to assess how candidate vaccines and infection influence the ontogenies of Envelope (Env)-specific antibodies is critical for the development of an HIV vaccine. Here we use two nonhuman primate models to compare the roles of antigen persistence, diversity and innate immunity. We perform longitudinal analyses of HIV Env-specific B-cell receptor responses to SHIV(AD8) infection and Env protein vaccination with eight different adjuvants. A subset of the SHIV(AD8)-infected animals with higher viral loads and greater Env diversity show increased neutralization associated with increasing somatic hypermutation (SHM) levels over time. The use of adjuvants results in increased ELISA titres but does not affect the mean SHM levels or CDR H3 lengths. Our study shows how the ontogeny of Env-specific B cells can be tracked, and provides insights into the requirements for developing neutralizing antibodies that should facilitate translation to human vaccine studies.
[Mh] Termos MeSH primário: Vacinas contra a AIDS/imunologia
Adjuvantes Imunológicos
Infecções por HIV/prevenção & controle
HIV-1/imunologia
Imunoglobulinas/imunologia
RNA Mensageiro/metabolismo
Síndrome de Imunodeficiência Adquirida dos Símios/prevenção & controle
Vírus da Imunodeficiência Símia/imunologia
Produtos do Gene env do Vírus da Imunodeficiência Humana/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Neutralizantes/imunologia
Linfócitos B/imunologia
Sequência de Bases
Infecções por HIV/imunologia
Imunoglobulinas/genética
Infecções por Lentivirus/imunologia
Infecções por Lentivirus/prevenção & controle
Lentivirus de Primatas/imunologia
Estudos Longitudinais
Macaca mulatta
Dados de Sequência Molecular
RNA Viral/análise
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (AIDS Vaccines); 0 (Adjuvants, Immunologic); 0 (Antibodies, Neutralizing); 0 (Immunoglobulins); 0 (RNA, Messenger); 0 (RNA, Viral); 0 (env Gene Products, Human Immunodeficiency Virus)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150411
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms7565


  9 / 91 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25620704
[Au] Autor:Sauter D; Hotter D; Van Driessche B; Stürzel CM; Kluge SF; Wildum S; Yu H; Baumann B; Wirth T; Plantier JC; Leoz M; Hahn BH; Van Lint C; Kirchhoff F
[Ad] Endereço:Institute of Molecular Virology, Ulm University Medical Center, 89081 Ulm, Germany. Electronic address: daniel.sauter@uni-ulm.de.
[Ti] Título:Differential regulation of NF-κB-mediated proviral and antiviral host gene expression by primate lentiviral Nef and Vpu proteins.
[So] Source:Cell Rep;10(4):586-99, 2015 Feb 03.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NF-κB is essential for effective transcription of primate lentiviral genomes and also activates antiviral host genes. Here, we show that the early protein Nef of most primate lentiviruses enhances NF-κB activation. In contrast, the late protein Vpu of HIV-1 and its simian precursors inhibits activation of NF-κB, even in the presence of Nef. Although this effect of Vpu did not correlate with its ability to interact with ß-TrCP, it involved the stabilization of IκB and reduced nuclear translocation of p65. Interestingly, however, Vpu did not affect casein kinase II-mediated phosphorylation of p65. Lack of Vpu was associated with increased NF-κB activation and induction of interferon and interferon-stimulated genes (ISGs) in HIV-1-infected T cells. Thus, HIV-1 and its simian precursors employ Nef to boost NF-κB activation early during the viral life cycle to initiate proviral transcription, while Vpu is used to downmodulate NF-κB-dependent expression of ISGs at later stages.
[Mh] Termos MeSH primário: Lentivirus de Primatas/metabolismo
NF-kappa B/metabolismo
Proteínas Virais/metabolismo
[Mh] Termos MeSH secundário: Animais
Expressão Gênica
HIV-1/genética
HIV-1/metabolismo
Quinase I-kappa B/metabolismo
Proteínas I-kappa B/metabolismo
Imunidade Inata/fisiologia
Lentivirus de Primatas/genética
Proteínas Virais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (I-kappa B Proteins); 0 (NF-kappa B); 0 (Viral Proteins); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150127
[St] Status:MEDLINE


  10 / 91 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25463599
[Au] Autor:Qian J; Le Duff Y; Wang Y; Pan Q; Ding S; Zheng YM; Liu SL; Liang C
[Ad] Endereço:Lady Davis Institute, Jewish General Hospital, Montreal, Quebec, Canada H3T 1E2; Department of Medicine, McGill University, Montreal, Quebec, Canada H3A 2B4.
[Ti] Título:Primate lentiviruses are differentially inhibited by interferon-induced transmembrane proteins.
[So] Source:Virology;474:10-8, 2015 Jan 01.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interferon-induced transmembrane (IFITM) proteins inhibit the entry of a large number of viruses. Not surprisingly, many viruses are refractory to this inhibition. In this study, we report that different strains of HIV and SIV are inhibited by human IFITM proteins to various degrees, with SIV of African green monkeys (SIV(AGM)) being mostly restricted by human IFITM2. Interestingly, SIV(AGM) is as much inhibited by human IFITM2 as by IFITM3 of its own host African green monkeys. Our data further demonstrate that the entry of SIV(AGM) is impaired by human IFITM2 and that this inhibition is overcome by the cholesterol-binding compound amphotericin B that also overcomes IFITM inhibition of influenza A viruses. These results suggest that IFITM proteins exploit similar mechanisms to inhibit the entry of both pH-independent primate lentiviruses and the pH-dependent influenza A viruses.
[Mh] Termos MeSH primário: Interações Hospedeiro-Patógeno/imunologia
Interferons/imunologia
Lentivirus de Primatas/patogenicidade
Proteínas de Membrana/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Células COS
Cercopithecus aethiops
Células HEK293
HIV/imunologia
HIV/patogenicidade
HIV/fisiologia
Seres Humanos
Vírus da Influenza A/imunologia
Vírus da Influenza A/patogenicidade
Vírus da Influenza A/fisiologia
Lentivirus de Primatas/imunologia
Lentivirus de Primatas/fisiologia
Proteínas de Membrana/genética
Dados de Sequência Molecular
Homologia de Sequência de Aminoácidos
Vírus da Imunodeficiência Símia/imunologia
Vírus da Imunodeficiência Símia/patogenicidade
Vírus da Imunodeficiência Símia/fisiologia
Células Vero
Internalização do Vírus
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 9008-11-1 (Interferons)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE



página 1 de 10 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