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[PMID]:26394054
[Au] Autor:Etienne L; Bibollet-Ruche F; Sudmant PH; Wu LI; Hahn BH; Emerman M
[Ad] Endereço:Divisions of Human Biology and Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
[Ti] Título:The Role of the Antiviral APOBEC3 Gene Family in Protecting Chimpanzees against Lentiviruses from Monkeys.
[So] Source:PLoS Pathog;11(9):e1005149, 2015 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cross-species transmissions of viruses from animals to humans are at the origin of major human pathogenic viruses. While the role of ecological and epidemiological factors in the emergence of new pathogens is well documented, the importance of host factors is often unknown. Chimpanzees are the closest relatives of humans and the animal reservoir at the origin of the human AIDS pandemic. However, despite being regularly exposed to monkey lentiviruses through hunting, chimpanzees are naturally infected by only a single simian immunodeficiency virus, SIVcpz. Here, we asked why chimpanzees appear to be protected against the successful emergence of other SIVs. In particular, we investigated the role of the chimpanzee APOBEC3 genes in providing a barrier to infection by most monkey lentiviruses. We found that most SIV Vifs, including Vif from SIVwrc infecting western-red colobus, the chimpanzee's main monkey prey in West Africa, could not antagonize chimpanzee APOBEC3G. Moreover, chimpanzee APOBEC3D, as well as APOBEC3F and APOBEC3H, provided additional protection against SIV Vif antagonism. Consequently, lentiviral replication in primary chimpanzee CD4(+) T cells was dependent on the presence of a lentiviral vif gene that could antagonize chimpanzee APOBEC3s. Finally, by identifying and functionally characterizing several APOBEC3 gene polymorphisms in both common chimpanzees and bonobos, we found that these ape populations encode APOBEC3 proteins that are uniformly resistant to antagonism by monkey lentiviruses.
[Mh] Termos MeSH primário: Citidina Desaminase/genética
Infecções por Lentivirus/genética
Pan troglodytes/imunologia
Pan troglodytes/virologia
Vírus da Imunodeficiência Símia/genética
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linfócitos T CD4-Positivos/imunologia
Citidina Desaminase/imunologia
Genes vif/genética
Haplorrinos
Lentivirus/genética
Infecções por Lentivirus/imunologia
Dados de Sequência Molecular
Filogenia
Reação em Cadeia da Polimerase
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.5.4.5 (Cytidine Deaminase)
[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:150923
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1005149


  2 / 118 MEDLINE  
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[PMID]:25428257
[Au] Autor:Elhadidy MM; Elkhatib WF
[Ad] Endereço:Department of Bacteriology,Mycology and Immunology,Faculty of Veterinary Medicine,Mansoura University,Mansoura,Egypt.
[Ti] Título:Multilocus genotypic characterization of Escherichia coli O157:H7 recovered from food sources.
[So] Source:Epidemiol Infect;143(11):2367-72, 2015 Aug.
[Is] ISSN:1469-4409
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Escherichia coli O157:H7 strains (n = 33) recovered from different food sources in Egypt were characterized using molecular assays to identify strain genotypes associated with various levels of pathogenic potential. Genotypic characterization included: lineage-specific polymorphism assay (LSPA-6), Shiga-toxin-encoding bacteriophage insertion site assay (SBI), clade 8 typing, Tir (A255 T) polymorphism, and variant analysis of Shiga toxin 2 gene (Stx 2a and Stx 2c), and anti-terminator Q genes (Q 933 and Q 21). Genotypes LI/II (76%), SBI 1 (60·6%), clade 8 (69·7%), Tir (255 T) (72·7%) and Stx 2c (45·5%) were found to be significantly more frequent compared to other genetic markers in the strains analysed. Multivariable analysis revealed a significant association between LPSA-6 and clade types as well as Tir (A255 T). To the best of our knowledge, this is the first study to report the characterization of these genetic markers in E. coli O157:H7 strains in the Middle East and Africa.
[Mh] Termos MeSH primário: DNA Bacteriano/genética
Escherichia coli O157/genética
Microbiologia de Alimentos
Fatores de Virulência/genética
[Mh] Termos MeSH secundário: Animais
Queijo/microbiologia
Egito
Infecções por Escherichia coli/microbiologia
Proteínas de Escherichia coli/genética
Genes vif/genética
Genótipo
Seres Humanos
Carne/microbiologia
Leite/microbiologia
Receptores de Superfície Celular/genética
Toxina Shiga/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Escherichia coli Proteins); 0 (Receptors, Cell Surface); 0 (Tir protein, E coli); 0 (Virulence Factors); 75757-64-1 (Shiga Toxin)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:150701
[Lr] Data última revisão:
150701
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141128
[St] Status:MEDLINE
[do] DOI:10.1017/S0950268814003197


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[PMID]:24198285
[Au] Autor:Maeda K; Almofty SA; Singh SK; Eid MMA; Shimoda M; Ikeda T; Koito A; Pham P; Goodman MF; Sakaguchi N
[Ad] Endereço:Department of Immunology, Graduate School of Life Sciences, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto 860-8556, Japan.
[Ti] Título:GANP interacts with APOBEC3G and facilitates its encapsidation into the virions to reduce HIV-1 infectivity.
[So] Source:J Immunol;191(12):6030-6039, 2013 Dec 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ssDNA-dependent deoxycytidine deaminase apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G (A3G) is a potent restrictive factor against HIV-1 virus lacking viral-encoded infectivity factor (Vif) in CD4(+) T cells. A3G antiretroviral activity requires its encapsulation into HIV-1 virions. In this study, we show that germinal center-associated nuclear protein (GANP) is induced in activated CD4(+) T cells and physically interacts with A3G. Overexpression of GANP augments the A3G encapsidation into the virion-like particles and ΔVif HIV-1 virions. GANP is encapsidated in HIV-1 virion and modulates A3G packaging into the cores together with cellular RNAs, including 7SL RNA, and with unspliced HIV-1 genomic RNA. GANP upregulation leads to a significant increase in A3G-catalyzed G→A hypermutation in the viral genome and suppression of HIV-1 infectivity in a single-round viral infection assay. Conversely, GANP knockdown caused a marked increase in HIV-1 infectivity in a multiple-round infection assay. The data suggest that GANP is a cellular factor that facilitates A3G encapsidation into HIV-1 virions to inhibit viral infectivity.
[Mh] Termos MeSH primário: Acetiltransferases/fisiologia
Linfócitos T CD4-Positivos/imunologia
Citidina Desaminase/fisiologia
HIV-1/fisiologia
Peptídeos e Proteínas de Sinalização Intracelular/fisiologia
Vírion/metabolismo
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G
Acetiltransferases/antagonistas & inibidores
Acetiltransferases/biossíntese
Acetiltransferases/química
Acetiltransferases/genética
Células Cultivadas
Citidina Desaminase/química
Genes vif
HIV-1/ultraestrutura
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/antagonistas & inibidores
Peptídeos e Proteínas de Sinalização Intracelular/biossíntese
Peptídeos e Proteínas de Sinalização Intracelular/química
Peptídeos e Proteínas de Sinalização Intracelular/genética
Ativação Linfocitária
Mutação
Mapeamento de Interação de Proteínas
RNA Guia/metabolismo
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
RNA Citoplasmático Pequeno/metabolismo
RNA Interferente Pequeno/farmacologia
RNA Viral/genética
RNA Viral/metabolismo
Partícula de Reconhecimento de Sinal/metabolismo
Regulação para Cima
Vírion/ultraestrutura
Virulência
Replicação Viral
Produtos do Gene vif do Vírus da Imunodeficiência Humana/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (7SL RNA); 0 (Intracellular Signaling Peptides and Proteins); 0 (RNA, Guide); 0 (RNA, Messenger); 0 (RNA, Small Cytoplasmic); 0 (RNA, Small Interfering); 0 (RNA, Viral); 0 (Signal Recognition Particle); 0 (vif Gene Products, Human Immunodeficiency Virus); 0 (vif protein, Human immunodeficiency virus 1); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.- (MCM3AP protein, human); EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:131108
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1302057


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[PMID]:24074935
[Au] Autor:Eckers JC; Kalen AL; Xiao W; Sarsour EH; Goswami PC
[Ad] Endereço:Free Radical and Radiation Biology Division, Department of Radiation Oncology, University of Iowa, Iowa City, Iowa.
[Ti] Título:Selenoprotein P inhibits radiation-induced late reactive oxygen species accumulation and normal cell injury.
[So] Source:Int J Radiat Oncol Biol Phys;87(3):619-25, 2013 Nov 01.
[Is] ISSN:1879-355X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Radiation is a common mode of cancer therapy whose outcome is often limited because of normal tissue toxicity. We have shown previously that the accumulation of radiation-induced late reactive oxygen species (ROS) precedes cell death, suggesting that metabolic oxidative stress could regulate cellular radiation response. The purpose of this study was to investigate whether selenoprotein P (SEPP1), a major supplier of selenium to tissues and an antioxidant, regulates late ROS accumulation and toxicity in irradiated normal human fibroblasts (NHFs). METHODS AND MATERIALS: Flow cytometry analysis of cell viability, cell cycle phase distribution, and dihydroethidium oxidation, along with clonogenic assays, were used to measure oxidative stress and toxicity. Human antioxidant mechanisms array and quantitative real-time polymerase chain reaction assays were used to measure gene expression during late ROS accumulation in irradiated NHFs. Sodium selenite addition and SEPP1 overexpression were used to determine the causality of SEPP1 regulating late ROS accumulation and toxicity in irradiated NHFs. RESULTS: Irradiated NHFs showed late ROS accumulation (4.5-fold increase from control; P<.05) that occurs after activation of the cell cycle checkpoint pathways and precedes cell death. The mRNA levels of CuZn- and Mn-superoxide dismutase, catalase, peroxiredoxin 3, and thioredoxin reductase 1 increased approximately 2- to 3-fold, whereas mRNA levels of cold shock domain containing E1 and SEPP1 increased more than 6-fold (P<.05). The addition of sodium selenite before the radiation treatment suppressed toxicity (45%; P<.05). SEPP1 overexpression suppressed radiation-induced late ROS accumulation (35%; P<.05) and protected NHFs from radiation-induced toxicity (58%; P<.05). CONCLUSION: SEPP1 mitigates radiation-induced late ROS accumulation and normal cell injury.
[Mh] Termos MeSH primário: Lesões por Radiação/prevenção & controle
Espécies Reativas de Oxigênio/metabolismo
Selenoproteína P/fisiologia
[Mh] Termos MeSH secundário: Pontos de Checagem do Ciclo Celular/fisiologia
Pontos de Checagem do Ciclo Celular/efeitos da radiação
Morte Celular
Sobrevivência Celular
Relação Dose-Resposta à Radiação
Etídio/análogos & derivados
Etídio/metabolismo
Fibroblastos/metabolismo
Fibroblastos/efeitos da radiação
Genes vif
Seres Humanos
Estresse Oxidativo/genética
Reação em Cadeia da Polimerase em Tempo Real
Selenoproteína P/genética
Selenoproteína P/metabolismo
Selenito de Sódio/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 0 (Selenoprotein P); 104821-25-2 (dihydroethidium); EN464416SI (Ethidium); HIW548RQ3W (Sodium Selenite)
[Em] Mês de entrada:1311
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131001
[St] Status:MEDLINE


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[PMID]:22807680
[Au] Autor:Refsland EW; Hultquist JF; Harris RS
[Ad] Endereço:Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, Minnesota, United States of America.
[Ti] Título:Endogenous origins of HIV-1 G-to-A hypermutation and restriction in the nonpermissive T cell line CEM2n.
[So] Source:PLoS Pathog;8(7):e1002800, 2012.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The DNA deaminase APOBEC3G converts cytosines to uracils in retroviral cDNA, which are immortalized as genomic strand G-to-A hypermutations by reverse transcription. A single round of APOBEC3G-dependent mutagenesis can be catastrophic, but evidence suggests that sublethal levels contribute to viral genetic diversity and the associated problems of drug resistance and immune escape. APOBEC3G exhibits an intrinsic preference for the second cytosine in a 5'CC dinucleotide motif leading to 5'GG-to-AG mutations. However, an additional hypermutation signature is commonly observed in proviral sequences from HIV-1 infected patients, 5'GA-to-AA, and it has been attributed controversially to one or more of the six other APOBEC3 deaminases. An unambiguous resolution of this problem has been difficult to achieve, in part due to dominant effects of protein over-expression. Here, we employ gene targeting to dissect the endogenous APOBEC3 contribution to Vif-deficient HIV-1 restriction and hypermutation in a nonpermissive T cell line CEM2n. We report that APOBEC3G-null cells, as predicted from previous studies, lose the capacity to inflict 5'GG-to-AG mutations. In contrast, APOBEC3F-null cells produced viruses with near-normal mutational patterns. Systematic knockdown of other APOBEC3 genes in an APOBEC3F-null background revealed a significant contribution from APOBEC3D in promoting 5'GA-to-AA hypermutations. Furthermore, Vif-deficient HIV-1 restriction was strong in parental CEM2n and APOBEC3D-knockdown cells, partially alleviated in APOBEC3G- or APOBEC3F-null cells, further alleviated in APOBEC3F-null/APOBEC3D-knockdown cells, and alleviated to the greatest extent in APOBEC3F-null/APOBEC3G-knockdown cells revealing clear redundancy in the HIV-1 restriction mechanism. We conclude that endogenous levels of APOBEC3D, APOBEC3F, and APOBEC3G combine to restrict Vif-deficient HIV-1 and cause the hallmark dinucleotide hypermutation patterns in CEM2n. Primary T lymphocytes express a similar set of APOBEC3 genes suggesting that the same repertoire may be important in vivo.
[Mh] Termos MeSH primário: Citidina Desaminase/metabolismo
Citosina Desaminase/metabolismo
Genes vif
HIV-1/genética
Mutação
Linfócitos T/virologia
Produtos do Gene vif do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Desaminase APOBEC-3G
Linhagem Celular
Citidina Desaminase/genética
Citosina Desaminase/genética
Variação Genética
Células HEK293
HIV-1/fisiologia
Seres Humanos
Mutagênese
Interferência de RNA
RNA Interferente Pequeno
Linfócitos T/citologia
Replicação Viral/genética
Produtos do Gene vif do Vírus da Imunodeficiência Humana/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (vif Gene Products, Human Immunodeficiency Virus); EC 3.5.4.1 (APOBEC3F protein, human); EC 3.5.4.1 (Cytosine Deaminase); EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (Cytidine Deaminase)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120719
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1002800


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[PMID]:22553496
[Au] Autor:Malim MH; Bieniasz PD
[Ad] Endereço:Department of Infectious Diseases, King's College London School of Medicine, Guy's Hospital, London Bridge, London SE1 9RT, United Kingdom. michael.malim@kcl.ac.uk
[Ti] Título:HIV Restriction Factors and Mechanisms of Evasion.
[So] Source:Cold Spring Harb Perspect Med;2(5):a006940, 2012 May.
[Is] ISSN:2157-1422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retroviruses have long been a fertile model for discovering host-pathogen interactions and their associated biological principles and processes. These advances have not only informed fundamental concepts of viral replication and pathogenesis but have also provided novel insights into host cell biology. This is illustrated by the recent descriptions of host-encoded restriction factors that can serve as effective inhibitors of retroviral replication. Here, we review our understanding of the three restriction factors that have been widely shown to be potent inhibitors of HIV-1: namely, APOBEC3G, TRIM5α, and tetherin. In each case, we discuss how these unrelated proteins were identified, the mechanisms by which they inhibit replication, the means used by HIV-1 to evade their action, and their potential contributions to viral pathogenesis as well as inter- and intraspecies transmission.
[Mh] Termos MeSH primário: Antígenos CD/fisiologia
Proteínas de Transporte/fisiologia
Citosina Desaminase/fisiologia
Infecções por HIV/virologia
HIV-1/fisiologia
[Mh] Termos MeSH secundário: Proteínas Ligadas por GPI/antagonistas & inibidores
Proteínas Ligadas por GPI/fisiologia
Genes vif/genética
Infecções por HIV/genética
HIV-1/genética
Interações Hospedeiro-Patógeno
Seres Humanos
Mutação/genética
Proteínas Virais Reguladoras e Acessórias/antagonistas & inibidores
Proteínas Virais Reguladoras e Acessórias/fisiologia
Replicação Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (BST2 protein, human); 0 (Carrier Proteins); 0 (GPI-Linked Proteins); 0 (TRIM5 protein, human); 0 (Viral Regulatory and Accessory Proteins); EC 3.5.4.1 (APOBEC3 protein, human); EC 3.5.4.1 (Cytosine Deaminase)
[Em] Mês de entrada:1306
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120504
[St] Status:MEDLINE
[do] DOI:10.1101/cshperspect.a006940


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[PMID]:22387557
[Au] Autor:Mudd PA; Ericsen AJ; Burwitz BJ; Wilson NA; O'Connor DH; Hughes AL; Watkins DI
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, WI 53711, USA.
[Ti] Título:Escape from CD8(+) T cell responses in Mamu-B*00801(+) macaques differentiates progressors from elite controllers.
[So] Source:J Immunol;188(7):3364-70, 2012 Apr 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A small number of HIV-infected individuals known as elite controllers experience low levels of chronic phase viral replication and delayed progression to AIDS. Specific HLA class I alleles are associated with elite control, implicating CD8(+) T lymphocytes in the establishment of these low levels of viral replication. Most HIV-infected individuals that express protective HLA class I alleles, however, do not control viral replication. Approximately 50% of Mamu-B*00801(+) Indian rhesus macaques control SIVmac239 replication in the chronic phase in a manner that resembles elite control in humans. We followed both the immune response and viral evolution in SIV-infected Mamu-B*00801(+) animals to better understand the role of CD8(+) T lymphocytes during the acute phase of viral infection, when viral control status is determined. The virus escaped from immunodominant Vif and Nef Mamu-B*00801-restricted CD8(+) T lymphocyte responses during the critical early weeks of acute infection only in progressor animals that did not control viral replication. Thus, early CD8(+) T lymphocyte escape is a hallmark of Mamu-B*00801(+) macaques who do not control viral replication. By contrast, virus in elite controller macaques showed little evidence of variation in epitopes recognized by immunodominant CD8(+) T lymphocytes, implying that these cells play a role in viral control.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Antígenos de Histocompatibilidade Classe I/imunologia
Evasão da Resposta Imune/imunologia
Macaca mulatta/imunologia
Síndrome de Imunodeficiência Adquirida dos Símios/imunologia
Vírus da Imunodeficiência Símia/imunologia
Subpopulações de Linfócitos T/imunologia
Viremia/imunologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência Consenso
Progressão da Doença
Resistência à Doença/genética
Resistência à Doença/imunologia
Produtos do Gene nef/imunologia
Produtos do Gene vif/imunologia
Genes nef
Genes vif
Antígenos de Histocompatibilidade Classe I/genética
Evasão da Resposta Imune/genética
Epitopos Imunodominantes/imunologia
Macaca mulatta/genética
Dados de Sequência Molecular
RNA Viral/genética
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Síndrome de Imunodeficiência Adquirida dos Símios/genética
Vírus da Imunodeficiência Símia/genética
Vírus da Imunodeficiência Símia/fisiologia
Especificidade do Receptor de Antígeno de Linfócitos T
Fatores de Tempo
Carga Viral
Viremia/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Gene Products, nef); 0 (Gene Products, vif); 0 (Histocompatibility Antigens Class I); 0 (Immunodominant Epitopes); 0 (RNA, Viral)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120306
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1102470


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[PMID]:22041522
[Au] Autor:Hung CF; Lung FW; Hung TH; Chong MY; Wu CK; Wen JK; Lin PY
[Ad] Endereço:Department of Psychiatry, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan.
[Ti] Título:Monoamine oxidase A gene polymorphism and suicide: an association study and meta-analysis.
[So] Source:J Affect Disord;136(3):643-9, 2012 Feb.
[Is] ISSN:1573-2517
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Abnormalities in brain monoamine transmission have been implicated in the pathogenesis of suicidal behavior. Studies examining the association between monoamine oxidase A (MAOA)-uVNTR polymorphism and suicide revealed inconsistent findings. This study aims to evaluate the possible association between the MAOA-uVNTR polymorphism and suicidal behaviors by examining our own subjects and conducting a meta-analytic review. METHODS: 373 unrelated psychiatric patients (including 160 suicide attempters and 213 non-suicide attempters) were genotyped for the MAOA-uVNTR polymorphism. A meta-analysis was then performed by pooling data from seven case-control association studies by random effects model. RESULTS: Our results indicate that there is no association between the MAOA-uVNTR polymorphism and suicide attempts in both genders. It also reveals that there is no association with violent suicide attempts. In the meta-analysis, there is no association between the polymorphism and suicidal behaviors. Also, there is no difference in the allelic distribution between psychiatric patients with and without suicidal behaviors. Limitations Our study was constrained by the insufficient information about environmental risk factors of suicide. CONCLUSIONS: Our study is the first one to use meta-analysis in exploring the role of the MAOA-uVNTR polymorphism in suicidal behavior in psychiatric patients. No significant association was found in our study, suggesting MAOA-uVNTR polymorphism is unlikely to contribute significantly to suicide behavior. Further studies investigating the gene-environment interaction or focusing on the genetic risk factors of endophenotypes of suicidal behaviors are warranted.
[Mh] Termos MeSH primário: Transtorno Bipolar/genética
Transtorno Depressivo Maior/genética
Monoaminoxidase/genética
Esquizofrenia/genética
Suicídio
[Mh] Termos MeSH secundário: Adulto
Alelos
Transtorno Bipolar/psicologia
Estudos de Casos e Controles
China
Transtorno Depressivo Maior/psicologia
Feminino
Interação Gene-Ambiente
Genes vif
Genótipo
Seres Humanos
Masculino
Polimorfismo Genético
Fatores de Risco
Psicologia do Esquizofrênico
Tentativa de Suicídio
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 1.4.3.4 (Monoamine Oxidase)
[Em] Mês de entrada:1210
[Cu] Atualização por classe:120221
[Lr] Data última revisão:
120221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111102
[St] Status:MEDLINE
[do] DOI:10.1016/j.jad.2011.10.013


  9 / 118 MEDLINE  
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[PMID]:21741003
[Au] Autor:Lever RA; Lever AM
[Ad] Endereço:Department of Medicine, Addenbrooke's Hospital, Cambridge, UK.
[Ti] Título:Intracellular defenses against HIV, viral evasion and novel therapeutic approaches.
[So] Source:J Formos Med Assoc;110(6):350-62, 2011 Jun.
[Is] ISSN:0929-6646
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:Human immunodeficiency virus (HIV), the causative agent of AIDS, is a retrovirus. It is estimated that, while in the cell, it interacts with almost 10% of cellular proteins. Several of these have evolved to protect the cell from infection with retroviruses and are known as "restriction factors". Restriction factors tell us much about how the virus functions and open up new paradigms for exploring novel antiviral therapeutics. This article gives an update on the three best studied restriction factors, their putative mechanisms of action and how the virus has overcome their effects, together with an indication of novel therapeutic approaches based on this knowledge.
[Mh] Termos MeSH primário: Síndrome de Imunodeficiência Adquirida
Antivirais
HIV
Imunidade Inata/genética
[Mh] Termos MeSH secundário: Síndrome de Imunodeficiência Adquirida/tratamento farmacológico
Síndrome de Imunodeficiência Adquirida/imunologia
Síndrome de Imunodeficiência Adquirida/metabolismo
Síndrome de Imunodeficiência Adquirida/virologia
Antígenos CD/metabolismo
Antivirais/farmacologia
Antivirais/uso terapêutico
Capsídeo/metabolismo
Proteínas de Transporte/metabolismo
Ensaios Clínicos como Assunto
Citosina Desaminase/metabolismo
Proteínas Ligadas por GPI/metabolismo
Genes vif
Estudo de Associação Genômica Ampla
HIV/efeitos dos fármacos
HIV/genética
HIV/fisiologia
Seres Humanos
Replicação Viral/efeitos dos fármacos
Replicação Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antiviral Agents); 0 (BST2 protein, human); 0 (Carrier Proteins); 0 (GPI-Linked Proteins); 0 (TRIM5 protein, human); EC 3.5.4.1 (APOBEC3 protein, human); EC 3.5.4.1 (Cytosine Deaminase)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110712
[St] Status:MEDLINE
[do] DOI:10.1016/S0929-6646(11)60053-3


  10 / 118 MEDLINE  
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[PMID]:21576818
[Au] Autor:Wheeler LA; Trifonova R; Vrbanac V; Basar E; McKernan S; Xu Z; Seung E; Deruaz M; Dudek T; Einarsson JI; Yang L; Allen TM; Luster AD; Tager AM; Dykxhoorn DM; Lieberman J
[Ad] Endereço:Immune Disease Institute and Program in Cellular and Molecular Medicine, Children's Hospital Boston, Harvard Medical School, Boston, Massachusetts, USA.
[Ti] Título:Inhibition of HIV transmission in human cervicovaginal explants and humanized mice using CD4 aptamer-siRNA chimeras.
[So] Source:J Clin Invest;121(6):2401-12, 2011 Jun.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The continued spread of the HIV epidemic underscores the need to interrupt transmission. One attractive strategy is a topical vaginal microbicide. Sexual transmission of herpes simplex virus type 2 (HSV-2) in mice can be inhibited by intravaginal siRNA application. To overcome the challenges of knocking down gene expression in immune cells susceptible to HIV infection, we used chimeric RNAs composed of an aptamer fused to an siRNA for targeted gene knockdown in cells bearing an aptamer-binding receptor. Here, we showed that CD4 aptamer-siRNA chimeras (CD4-AsiCs) specifically suppress gene expression in CD4⁺ T cells and macrophages in vitro, in polarized cervicovaginal tissue explants, and in the female genital tract of humanized mice. CD4-AsiCs do not activate lymphocytes or stimulate innate immunity. CD4-AsiCs that knock down HIV genes and/or CCR5 inhibited HIV infection in vitro and in tissue explants. When applied intravaginally to humanized mice, CD4-AsiCs protected against HIV vaginal transmission. Thus, CD4-AsiCs could be used as the active ingredient of a microbicide to prevent HIV sexual transmission.
[Mh] Termos MeSH primário: Aptâmeros de Nucleotídeos/uso terapêutico
Antígenos CD4/metabolismo
Linfócitos T CD4-Positivos/efeitos dos fármacos
Colo do Útero/efeitos dos fármacos
Genes gag
Genes vif
Infecções por HIV/prevenção & controle
Macrófagos/efeitos dos fármacos
RNA Interferente Pequeno/uso terapêutico
Receptores CCR5/genética
Quimeras de Transplante/virologia
Vagina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Administração Intravaginal
Animais
Aptâmeros de Nucleotídeos/administração & dosagem
Sequência de Bases
Antígenos CD4/genética
Linfócitos T CD4-Positivos/imunologia
Polaridade Celular
Células Cultivadas/efeitos dos fármacos
Células Cultivadas/metabolismo
Colo do Útero/virologia
Avaliação Pré-Clínica de Medicamentos
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Infecções por HIV/transmissão
Seres Humanos
Macrófagos/imunologia
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Dados de Sequência Molecular
Técnicas de Cultura de Órgãos
RNA Interferente Pequeno/administração & dosagem
Especificidade da Espécie
Quimeras de Transplante/imunologia
Vagina/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (CD4 Antigens); 0 (RNA, Small Interfering); 0 (Receptors, CCR5)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:110518
[St] Status:MEDLINE



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