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  1 / 284618 MEDLINE  
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[PMID]:25395177
[Au] Autor:Wakeham K; Johnston WT; Nalwoga A; Webb EL; Mayanja BN; Miley W; Elliott AM; Whitby D; Newton R
[Ad] Dirección:Medical Research Council/Uganda Virus Research Institute, Uganda Research Unit on AIDS, Entebbe, Uganda; Epidemiology and Cancer Statistics Group, Department of Health Sciences, University of York, Heslington, York, United Kingdom; Institute of Cancer Research, University of Glasgow, Scotland, United Kingdom.
[Ti] Título:Trends in Kaposi's sarcoma-associated Herpesvirus antibodies prior to the development of HIV-associated Kaposi's sarcoma: a nested case-control study.
[So] Fuente:Int J Cancer;136(12):2822-30, 2015 Jun 15.
[Is] ISSN:1097-0215
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:HIV-associated Kaposi's sarcoma (KS) is a public health challenge in sub-Saharan Africa since both the causative agent, Kaposi's sarcoma associated-herpesvirus (KSHV), and the major risk factor, HIV, are prevalent. In a nested case-control study within a long-standing clinical cohort in rural Uganda, we used stored sera to examine the evolution of antibody titres against the KSHV antigens K8.1 and latency-associated nuclear antigen (LANA) among 30 HIV-infected subjects who subsequently developed HIV-related KS (cases) and among 108 matched HIV/KSHV coinfected controls who did not develop KS. Throughout the 6 years prior to diagnosis, antibody titres to K8.1 and LANA were significantly higher among cases than controls (p < 0.0001), and titres increased prior to diagnosis in the cases. K8.1 titres differed more between KS cases and controls, compared to LANA titres. These differences in titre between cases and controls suggest a role for lytic viral replication in the pathogenesis of HIV-related KS in this setting.
[Mh] Términos MeSH primario: Anticuerpos Antivirales/inmunología
Infecciones por VIH/inmunología
Herpesvirus Humano 8/inmunología
Sarcoma de Kaposi/inmunología
[Mh] Términos MeSH secundario: Adulto
Anticuerpos Antivirales/sangre
Antígenos Virales/inmunología
Estudios de Casos y Controles
Coinfección/sangre
Coinfección/inmunología
Coinfección/virología
Ensayo de Inmunoadsorción Enzimática
Femenino
Glicoproteínas/inmunología
Infecciones por VIH/complicaciones
Humanos
Masculino
Proteínas Nucleares/inmunología
Sarcoma de Kaposi/complicaciones
Sarcoma de Kaposi/diagnóstico
Factores de Tiempo
Uganda
Proteínas Virales/inmunología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Antibodies, Viral); 0 (Antigens, Viral); 0 (Glycoproteins); 0 (K8.1 protein, Human herpesvirus 8); 0 (Nuclear Proteins); 0 (Viral Proteins); 0 (latency-associated nuclear antigen)
[Em] Mes de ingreso:1506
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150413
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.29329


  2 / 284618 MEDLINE  
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[PMID]:25505075
[Au] Autor:Donahue JP; Levinson RT; Sheehan JH; Sutton L; Taylor HE; Meiler J; D'Aquila RT; Song C
[Ad] Dirección:Division of Infectious Diseases, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA....
[Ti] Título:Genetic analysis of the localization of APOBEC3F to human immunodeficiency virus type 1 virion cores.
[So] Fuente:J Virol;89(4):2415-24, 2015 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: Members of the APOBEC3 family of cytidine deaminases vary in their proportions of a virion-incorporated enzyme that is localized to mature retrovirus cores. We reported previously that APOBEC3F (A3F) was highly localized into mature human immunodeficiency virus type 1 (HIV-1) cores and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core localization (C. Song, L. Sutton, M. Johnson, R. D'Aquila, J. Donahue, J Biol Chem 287:16965-16974, 2012, http://dx.doi.org/10.1074/jbc.M111.310839). We have now determined an additional genetic determinant(s) for A3F localization to HIV-1 cores. We found that one pair of leucines in each of A3F's C-terminal and N-terminal CD domains jointly determined the degree of localization of A3F into HIV-1 virion cores. These are A3F L306/L368 (C-terminal domain) and A3F L122/L184 (N-terminal domain). Alterations to one of these specific leucine residues in either of the two A3F CD domains (A3F L368A, L122A, and L184A) decreased core localization and diminished HIV restriction without changing virion packaging. Furthermore, double mutants in these leucine residues in each of A3F's two CD domains (A3F L368A plus L184A or A3F L368A plus L122A) still were packaged into virions but completely lost core localization and anti-HIV activity. HIV virion core localization of A3F is genetically separable from its virion packaging, and anti-HIV activity requires some core localization. IMPORTANCE: Specific leucine-leucine interactions are identified as necessary for A3F's core localization and anti-HIV activity but not for its packaging into virions. Understanding these signals may lead to novel strategies to enhance core localization that may augment effects of A3F against HIV and perhaps of other A3s against retroviruses, parvoviruses, and hepatitis B virus.
[Mh] Términos MeSH primario: Citosina Desaminasa/análisis
Citosina Desaminasa/genética
VIH-1/fisiología
Ensamble de Virus
[Mh] Términos MeSH secundario: Línea Celular
Citosina Desaminasa/inmunología
Análisis Mutacional de ADN
Genes Reporteros
VIH-1/química
VIH-1/inmunología
Humanos
Luciferasas/análisis
Modelos Moleculares
Mutagénesis Sitio-Dirigida
Mutación Missense
Coloración y Etiquetado
beta-Galactosidasa/análisis
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nombre de substancia:
EC 1.13.12.- (Luciferases); EC 3.2.1.23 (beta-Galactosidase); EC 3.5.4.1 (APOBEC3F protein, human); EC 3.5.4.1 (Cytosine Deaminase)
[Em] Mes de ingreso:1504
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150127
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01981-14


  3 / 284618 MEDLINE  
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[PMID]:25505066
[Au] Autor:Yu H; Khalid M; Heigele A; Schmökel J; Usmani SM; van der Merwe J; Münch J; Silvestri G; Kirchhoff F
[Ad] Dirección:Institute of Molecular Virology, Ulm University Medical Center, Ulm, Germany....
[Ti] Título:Lentiviral Nef proteins manipulate T cells in a subset-specific manner.
[So] Fuente:J Virol;89(4):1986-2001, 2015 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: The role of the accessory viral Nef protein as a multifunctional manipulator of the host cell that is required for effective replication of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) in vivo is well established. It is unknown, however, whether Nef manipulates all or just specific subsets of CD4(+) T cells, which are the main targets of virus infection and differ substantially in their state of activation and importance for a functional immune system. Here, we analyzed the effect of Nef proteins differing in their T cell receptor (TCR)-CD3 downmodulation function in HIV-infected human lymphoid aggregate cultures and peripheral blood mononuclear cells. We found that Nef efficiently downmodulates TCR-CD3 in naive and memory CD4(+) T cells and protects the latter against apoptosis. In contrast, highly proliferative CD45RA(+) CD45RO(+) CD4(+) T cells were main producers of infectious virus but largely refractory to TCR-CD3 downmodulation. Such T cell subset-specific differences were also observed for Nef-mediated modulation of CD4 but not for enhancement of virion infectivity. Our results indicate that Nef predominantly modulates surface receptors on CD4(+) T cell subsets that are not already fully permissive for viral replication. As a consequence, Nef-mediated downmodulation of TCR-CD3, which distinguishes most primate lentiviruses from HIV type 1 (HIV-1) and its vpu-containing simian precursors, may promote a selective preservation of central memory CD4(+) T cells, which are critical for the maintenance of a functional immune system. IMPORTANCE: The Nef proteins of human and simian immunodeficiency viruses manipulate infected CD4(+) T cells in multiple ways to promote viral replication and immune evasion in vivo. Here, we show that some effects of Nef are subset specific. Downmodulation of CD4 and TCR-CD3 is highly effective in central memory CD4(+) T cells, and the latter Nef function protects this T cell subset against apoptosis. In contrast, highly activated/proliferating CD4(+) T cells are largely refractory to receptor downmodulation but are main producers of infectious HIV-1. Nef-mediated enhancement of virion infectivity, however, was observed in all T cell subsets examined. Our results provide new insights into how primate lentiviruses manipulate their target cells and suggest that the TCR-CD3 downmodulation function of Nef may promote a selective preservation of memory CD4(+) T cells, which are critical for immune function, but has little effect on activated/proliferating CD4(+) T cells, which are the main targets for viral replication.
[Mh] Términos MeSH primario: Linfocitos T CD4-Positivos/virología
VIH-1/inmunología
Subgrupos de Linfocitos T/virología
Productos del Gen nef del Virus de la Inmunodeficiencia Humana/metabolismo
[Mh] Términos MeSH secundario: Animales
Antígenos CD3/análisis
Antígenos CD45/análisis
Apoptosis
Linfocitos T CD4-Positivos/inmunología
Supervivencia Celular
Humanos
Receptores de Antígenos de Linfocitos T/análisis
Subgrupos de Linfocitos T/inmunología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Antigens, CD3); 0 (Receptors, Antigen, T-Cell); 0 (nef Gene Products, Human Immunodeficiency Virus); 0 (nef protein, Human immunodeficiency virus 1); EC 3.1.3.48 (Antigens, CD45); EC 3.1.3.48 (PTPRC protein, human)
[Em] Mes de ingreso:1504
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150127
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.03104-14


  4 / 284618 MEDLINE  
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[PMID]:25473059
[Au] Autor:Wu F; Ourmanov I; Riddick N; Matsuda K; Whitted S; Plishka RJ; Buckler-White A; Starost MF; Hirsch VM
[Ad] Dirección:Laboratory of Molecular Microbiology, NIAID, NIH, Bethesda, Maryland, USA....
[Ti] Título:TRIM5α restriction affects clinical outcome and disease progression in simian immunodeficiency virus-infected rhesus macaques.
[So] Fuente:J Virol;89(4):2233-40, 2015 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: Tripartite motif-containing protein 5α (TRIM5α) is considered to be a potential target for cell-based gene modification therapy against human immunodeficiency virus type 1 (HIV-1) infection. In the present study, we used a relevant rhesus macaque model of infection with simian immunodeficiency virus from sooty mangabey (SIVsm) to evaluate the effect of TRIM5α restriction on clinical outcome. For macaques expressing a restrictive TRIM5 genotype, the disease outcomes of those infected with the wild-type TRIM-sensitive SIVsm strain and those infected with a virus with escape mutations in the capsid were compared. We found that TRIM5α restriction significantly delayed disease progression and improved the survival rate of SIV-infected macaques, supporting the feasibility of exploiting TRIM5α as a target for gene therapy against HIV-1. Furthermore, we also found that preservation of memory CD4 T cells was associated with protection by TRIM5α restriction, suggesting memory CD4 T cells or their progenitor cells as an ideal target for gene modification. Despite the significant effect of TRIM5α restriction on survival, SIV escape from TRIM5α restriction was also observed; therefore, this may not be an effective stand-alone strategy and may require combination with other targets. IMPORTANCE: Recent studies suggest that it may be feasible not only to suppress viral replication with antiviral drugs but also potentially to eliminate or "cure" human immunodeficiency virus (HIV) infection. One approach being explored is the use of gene therapy to introduce genes that can restrict HIV replication, including a restrictive version of the host factor TRIM5α. TRIM5 was identified as a factor that restricts HIV replication in macaque cells. The rhesus gene is polymorphic, and some alleles are restrictive for primary SIVsm isolates, although escape mutations arise late in infection. Introduction of these escape mutations into the parental virus conferred resistance to TRIM5 on macaques. The present study evaluated these animals for long-term outcomes and found that TRIM5α restriction significantly delayed disease progression and improved the survival rate of SIV-infected macaques, suggesting that this could be a valid gene therapy approach that could be adapted for HIV.
[Mh] Términos MeSH primario: Proteínas/inmunología
Proteínas/metabolismo
Síndrome de Inmunodeficiencia Adquirida del Simio/inmunología
Síndrome de Inmunodeficiencia Adquirida del Simio/patología
Virus de la Inmunodeficiencia de los Simios/inmunología
[Mh] Términos MeSH secundario: Animales
Linfocitos T CD4-Positivos/inmunología
Progresión de la Enfermedad
Genotipo
Memoria Inmunológica
Macaca mulatta
Proteínas/genética
Síndrome de Inmunodeficiencia Adquirida del Simio/mortalidad
Análisis de Supervivencia
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Proteins); 0 (TRIM5(alpha) protein, rhesus monkey)
[Em] Mes de ingreso:1504
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150127
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.02978-14


  5 / 284618 MEDLINE  
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[PMID]:25473058
[Au] Autor:Nunes-Cabaço H; Matoso P; Foxall RB; Tendeiro R; Pires AR; Carvalho T; Pinheiro AI; Soares RS; Sousa AE
[Ad] Dirección:Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal hcabaco@medicina.ulisboa.pt asousa@medicina.ulisboa.pt....
[Ti] Título:Thymic HIV-2 infection uncovers posttranscriptional control of viral replication in human thymocytes.
[So] Fuente:J Virol;89(4):2201-8, 2015 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: A unique HIV-host equilibrium exists in untreated HIV-2-infected individuals. This equilibrium is characterized by low to undetectable levels of viremia throughout the disease course, despite the establishment of disseminated HIV-2 reservoirs at levels comparable to those observed in untreated HIV-1 infection. Although the clinical spectrum is similar in the two infections, HIV-2 infection is associated with a much lower rate of CD4 T-cell decline and has a limited impact on the mortality of infected adults. Here we investigated HIV-2 infection of the human thymus, the primary organ for T-cell production. Human thymic tissue and suspensions of total or purified CD4 single-positive thymocytes were infected with HIV-2 or HIV-1 primary isolates using either CCR5 or CXCR4 coreceptors. We found that HIV-2 infected both thymic organ cultures and thymocyte suspensions, as attested to by the total HIV DNA and cell-associated viral mRNA levels. Nevertheless, thymocytes featured reduced levels of intracellular Gag viral protein, irrespective of HIV-2 coreceptor tropism and cell differentiation stage, in agreement with the low viral load in culture supernatants. Our data show that HIV-2 is able to infect the human thymus, but the HIV-2 replication cycle in thymocytes is impaired, providing a new model to identify therapeutic targets for viral replication control. IMPORTANCE: HIV-1 infects the thymus, leading to a decrease in CD4 T-cell production that contributes to the characteristic CD4 T-cell loss. HIV-2 infection is associated with a very low rate of progression to AIDS and is therefore considered a unique naturally occurring model of attenuated HIV disease. HIV-2-infected individuals feature low to undetectable plasma viral loads, in spite of the numbers of circulating infected T cells being similar to those found in patients infected with HIV-1. We assessed, for the first time, the direct impact of HIV-2 infection on the human thymus. We show that HIV-2 is able to infect the thymus but that the HIV-2 replication cycle in thymocytes is impaired. We propose that this system will be important to devise immunotherapies that target viral production, aiding the design of future therapeutic strategies for HIV control.
[Mh] Términos MeSH primario: VIH-2/fisiología
Interacciones Huésped-Patógeno
Timocitos/virología
Timo/virología
Replicación Viral
[Mh] Términos MeSH secundario: Adulto
Células Cultivadas
Preescolar
VIH-1/fisiología
Humanos
Lactante
Recién Nacido
Técnicas de Cultivo de Órganos
Timo/patología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mes de ingreso:1504
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150127
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.03047-14


  6 / 284618 MEDLINE  
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[PMID]:25473042
[Au] Autor:Mackelprang RD; Carrington M; Thomas KK; Hughes JP; Baeten JM; Wald A; Farquhar C; Fife K; Campbell MS; Kapiga S; Gao X; Mullins JI; Lingappa JR
[Ad] Dirección:Department of Global Health, University of Washington, Seattle, Washington, USA....
[Ti] Título:Host genetic and viral determinants of HIV-1 RNA set point among HIV-1 seroconverters from sub-saharan Africa.
[So] Fuente:J Virol;89(4):2104-11, 2015 Feb.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: We quantified the collective impact of source partner HIV-1 RNA levels, human leukocyte antigen (HLA) alleles, and innate responses through Toll-like receptor (TLR) alleles on the HIV-1 set point. Data came from HIV-1 seroconverters in African HIV-1 serodiscordant couple cohorts. Linear regression was used to determine associations with set point and R(2) to estimate variation explained by covariates. The strongest predictors of set point were HLA alleles (B*53:01, B*14:01, and B*27:03) and plasma HIV-1 levels of the transmitting partner, which explained 13% and 10% of variation in set point, respectively. HLA-A concordance between partners and TLR polymorphisms (TLR2 rs3804100 and TLR7 rs179012) also were associated with set point, explaining 6% and 5% of the variation, respectively. Overall, these factors and genital factors of the transmitter (i.e., male circumcision, bacterial vaginosis, and use of acyclovir) explained 46% of variation in set point. We found that both innate and adaptive immune responses, together with plasma HIV-1 levels of the transmitting partner, explain almost half of the variation in viral load set point. IMPORTANCE: After HIV-1 infection, uncontrolled virus replication leads to a rapid increase in HIV-1 concentrations. Once host immune responses develop, however, HIV-1 levels reach a peak and subsequently decline until they reach a stable level that may persist for years. This stable HIV-1 set point represents an equilibrium between the virus and host responses and is predictive of later disease progression and transmission potential. Understanding how host and virus factors interact to determine HIV-1 set point may elucidate novel mechanisms or biological pathways for treating HIV-1 infection. We identified host and virus factors that predict HIV-1 set point in people who recently acquired HIV-1, finding that both innate and adaptive immune responses, along with factors that likely influence HIV-1 virulence and inoculum, explain ∼46% of the variation in HIV-1 set point.
[Mh] Términos MeSH primario: Infecciones por VIH/inmunología
Infecciones por VIH/virología
VIH-1/aislamiento & purificación
Antígenos HLA/genética
ARN Viral/sangre
Carga Viral
[Mh] Términos MeSH secundario: África del Sur del Sahara
Estudios de Cohortes
Susceptibilidad a Enfermedades
Femenino
Infecciones por VIH/transmisión
Humanos
Masculino
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (HLA Antigens); 0 (RNA, Viral)
[Em] Mes de ingreso:1504
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150127
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01573-14


  7 / 284618 MEDLINE  
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[PMID]:25263953
[Au] Autor:Nabatanzi R; Bayigga L; Ssinabulya I; Kiragga A; Kambugu A; Olobo J; Joloba M; Kamya MR; Mayanja-Kizza H; Nakanjako D
[Ad] Dirección:Department of Medical Microbiology, Makerere University College of Health Sciences, Kampala, Uganda. Electronic address: rosemagala@yahoo.com....
[Ti] Título:Low antigen-specific CD4 T-cell immune responses despite normal absolute CD4 counts after long-term antiretroviral therapy an African cohort.
[So] Fuente:Immunol Lett;162(2 Pt B):264-72, 2014 Dec.
[Is] ISSN:1879-0542
[Cp] País de publicación:Netherlands
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: CD4 counts guide antiretroviral therapy (ART) initiation and prophylaxis for opportunistic infections. It is unclear whether normal CD4 counts translate to normalized immune responses among ART-treated adults. We compared antigen-specific CD4 T-cell immune responses among ART-treated adults with CD4≥500cells/µl, optimal immune responders (O-IR), and their age-matched healthy HIV-negative counterparts. METHODS: In a sample-based case-control study, cryopreserved peripheral blood mononuclear cells from 15 O-IR after 7 years of ART and 15 healthy controls, were analyzed for CD4+ T-cell proliferation using CFSE dye and cytokine production. RESULTS: CD4 T-cell proliferation, upon stimulation with PPD and pneumococcal polysaccharide antigen, was lower among O-IR relative to HIV-negative controls; p=0.016 and p=0.016 respectively. CD4 T-cell production of IL-2 was lower among O-IR relative to HIV-negative control p=0.002. CD4 T-cell proliferation upon stimulation with SEB and CMV antigens was similar among O-IR and HIV-negative controls p=0.971 and p=0.480, respectively, and so was IL-4 and IFN γ production; p=0.528 and p=0.892, respectively. CONCLUSION: Seven years of suppressive ART caused partial CD4 T-cell function recovery in an African HIV treatment cohort, despite restoration of CD4 T-cell counts to levels≥500cells/µl. The role innate immunity in the recovery of immune function during long-term ART should be investigated to guide decisions on continued prophylaxis against opportunistic infections.
[Mh] Términos MeSH primario: Infecciones Oportunistas Relacionadas con el SIDA/inmunología
Antígenos Bacterianos/inmunología
Linfocitos T CD4-Positivos/inmunología
Proliferación de la Célula
VIH-1/inmunología
Recuperación de la Función/inmunología
Streptococcus pneumoniae/inmunología
[Mh] Términos MeSH secundario: Infecciones Oportunistas Relacionadas con el SIDA/sangre
Infecciones Oportunistas Relacionadas con el SIDA/quimioterapia
Adulto
Antirretrovirales/administración & dosificación
Antígenos Bacterianos/farmacología
Recuento de Linfocito CD4
Linfocitos T CD4-Positivos/metabolismo
Linfocitos T CD4-Positivos/patología
Estudios de Casos y Controles
Femenino
Humanos
Interferón gamma/sangre
Interferón gamma/inmunología
Interleucina-2/sangre
Interleucina-2/inmunología
Interleucina-4/sangre
Interleucina-4/inmunología
Masculino
Mediana Edad
Recuperación de la Función/efectos de drogas
[Pt] Tipo de publicación:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Anti-Retroviral Agents); 0 (Antigens, Bacterial); 0 (IFNG protein, human); 0 (IL2 protein, human); 0 (IL4 protein, human); 0 (Interleukin-2); 207137-56-2 (Interleukin-4); 82115-62-6 (Interferon-gamma)
[Em] Mes de ingreso:1507
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:141205
[St] Status:MEDLINE


  8 / 284618 MEDLINE  
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[PMID]:24973214
[Au] Autor:Mueller AM; Yoon BH; Sadiq SA
[Ad] Dirección:From the Tisch Multiple Sclerosis Research Center of New York, New York, New York 10019.
[Ti] Título:Inhibition of hyaluronan synthesis protects against central nervous system (CNS) autoimmunity and increases CXCL12 expression in the inflamed CNS.
[So] Fuente:J Biol Chem;289(33):22888-99, 2014 Aug 15.
[Is] ISSN:1083-351X
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Hyaluronan (HA) may have proinflammatory roles in the context of CNS autoimmunity. It accumulates in demyelinated multiple sclerosis (MS) lesions, promotes antigen presentation, and enhances T-cell activation and proliferation. HA facilitates lymphocyte binding to vessels and CNS infiltration at the CNS vascular endothelium. Furthermore, HA signals through Toll-like receptors 2 and 4 to stimulate inflammatory gene expression. We assessed the role of HA in experimental autoimmune encephalomyelitis (EAE), an animal model of MS by administration of 4-methylumbelliferone (4MU), a well established inhibitor of HA synthesis. 4MU decreased hyaluronan synthesis in vitro and in vivo. It was protective in active EAE of C57Bl/6 mice, decreased spinal inflammatory infiltrates and spinal infiltration of Th1 cells, and increased differentiation of regulatory T-cells. In adoptive transfer EAE, feeding of 4MU to donor mice significantly decreased the encephalitogenicity of lymph node cells. The transfer of proteolipid protein (PLP)-stimulated lymph node cells to 4MU-fed mice resulted in a delayed EAE onset and delayed spinal T-cell infiltration. Expression of CXCL12, an anti-inflammatory chemokine, is reduced in MS patients in CSF cells and in spinal cord tissue during EAE. Hyaluronan suppressed production of CXCL12, whereas 4MU increased spinal CXCL12 in naive animals and during neuroinflammation. Neutralization of CXCR4, the most prominent receptor of CXCL12, by administration of AMD3100 diminished the protective impact of 4MU in adoptive transfer EAE. In conclusion, hyaluronan exacerbates CNS autoimmunity, enhances encephalitogenic T-cell responses, and suppresses the protective chemokine CXCL12 in CNS tissue. Inhibition of hyaluronan synthesis with 4MU protects against an animal model of MS and may represent an important therapeutic option in MS and other neuroinflammatory diseases.
[Mh] Términos MeSH primario: Sistema Nervioso Central/inmunología
Quimiocina CXCL12/inmunología
Encefalomielitis Autoinmune Experimental/inmunología
Regulación de la Expresión Génica/inmunología
Ácido Hialurónico/inmunología
[Mh] Términos MeSH secundario: Traslado Adoptivo
Animales
Fármacos Anti-VIH/farmacología
Sistema Nervioso Central/metabolismo
Quimiocina CXCL12/biosíntesis
Encefalomielitis Autoinmune Experimental/metabolismo
Encefalomielitis Autoinmune Experimental/patología
Femenino
Regulación de la Expresión Génica/efectos de drogas
Compuestos Heterocíclicos/farmacología
Ácido Hialurónico/biosíntesis
Inflamación/inmunología
Inflamación/metabolismo
Inflamación/patología
Ratones
Ratas
Linfocitos T Reguladores/inmunología
Linfocitos T Reguladores/metabolismo
Linfocitos T Reguladores/patología
Células TH1/inmunología
Células TH1/metabolismo
Células TH1/patología
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Anti-HIV Agents); 0 (CXCL12 protein, rat); 0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Heterocyclic Compounds); 155148-31-5 (JM 3100); 9004-61-9 (Hyaluronic Acid)
[Em] Mes de ingreso:1412
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140823
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M114.559583


  9 / 284618 MEDLINE  
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[PMID]:25050776
[Au] Autor:Ghosh AK; Schiltz GE; Rusere LN; Osswald HL; Walters DE; Amano M; Mitsuya H
[Ad] Dirección:Departments of Chemistry and Medicinal Chemistry, Purdue University, West Lafayette, IN 47907, USA. akghosh@purdue.edu.
[Ti] Título:Design and synthesis of potent macrocyclic HIV-1 protease inhibitors involving P1-P2 ligands.
[So] Fuente:Org Biomol Chem;12(35):6842-54, 2014 Sep 21.
[Is] ISSN:1477-0539
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:A series of potent macrocyclic HIV-1 protease inhibitors have been designed and synthesized. The compounds incorporated 16- to 19-membered macrocyclic rings between a nelfinavir-like P2 ligand and a tyrosine side chain containing a hydroxyethylamine sulfonamide isostere. All cyclic inhibitors are more potent than their corresponding acyclic counterparts. Saturated derivatives showed slight reduction of potency compared to the respective unsaturated derivatives. Compound containing a 16-membered ring as the P1-P2 ligand showed the most potent enzyme inhibitory and antiviral activity.
[Mh] Términos MeSH primario: Inhibidores de la Proteasa VIH/química
Nelfinavir/química
Sulfonamidas/química
[Mh] Términos MeSH secundario: Antivirales/síntesis química
Dominio Catalítico
Línea Celular
Diseño de Drogas
Evaluación Preclínica de Medicamentos
VIH-1/efectos de drogas
Humanos
Enlaces de Hidrógeno
Concentración 50 Inhibidora
Cinética
Ligandos
Espectroscopía de Resonancia Magnética
Modelos Moleculares
Estructura Molecular
Relación Estructura-Actividad
Tirosina/química
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Antiviral Agents); 0 (HIV Protease Inhibitors); 0 (Ligands); 0 (Sulfonamides); 42HK56048U (Tyrosine); HO3OGH5D7I (Nelfinavir); YO603Y8113 (darunavir)
[Em] Mes de ingreso:1506
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140813
[St] Status:MEDLINE
[do] DOI:10.1039/c4ob00738g


  10 / 284618 MEDLINE  
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[PMID]:25042339
[Au] Autor:Liu N; Qin B; Sun LQ; Yu F; Lu L; Jiang S; Lee KH; Xie L
[Ad] Dirección:Beijing Institute of Pharmacology & Toxicology, 27 Tai-Ping Road, Beijing 100850, China....
[Ti] Título:Physicochemical property-driven optimization of diarylaniline compounds as potent HIV-1 non-nucleoside reverse transcriptase inhibitors.
[So] Fuente:Bioorg Med Chem Lett;24(16):3719-23, 2014 Aug 15.
[Is] ISSN:1464-3405
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:Using physicochemical property-driven optimization, twelve new diarylaniline compounds (DAANs) (7a-h, 11a-b and 12a-b) were designed and synthesized. Among them, compounds 12a-b not only showed high potency (EC50 0.96-4.92 nM) against both wild-type and drug-resistant viral strains with the lowest fold change (FC 0.91 and 5.13), but also displayed acceptable drug-like properties based on aqueous solubility and lipophilicity (LE>0.3, LLE>5, LELP<10). The correlations between potency and physicochemical properties of these DAAN analogues are also described. Compounds 12a-b merit further development as potent clinical trial candidates against AIDS.
[Mh] Términos MeSH primario: Compuestos de Anilina/farmacología
Fármacos Anti-VIH/farmacología
Transcriptasa Inversa del VIH/antagonistas & inhibidores
VIH-1/efectos de drogas
Inhibidores de Transcriptasa Inversa/farmacología
[Mh] Términos MeSH secundario: Compuestos de Anilina/síntesis química
Compuestos de Anilina/química
Fármacos Anti-VIH/síntesis química
Fármacos Anti-VIH/química
Química Física
Relación Dosis-Respuesta a Droga
Transcriptasa Inversa del VIH/metabolismo
Pruebas de Sensibilidad Microbiana
Estructura Molecular
Inhibidores de Transcriptasa Inversa/síntesis química
Inhibidores de Transcriptasa Inversa/química
Relación Estructura-Actividad
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Aniline Compounds); 0 (Anti-HIV Agents); 0 (Reverse Transcriptase Inhibitors); EC 2.7.7.49 (HIV Reverse Transcriptase)
[Em] Mes de ingreso:1503
[Cu] Fecha actualización por clase:150815
[Lr] Fecha última revisión:150815
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140811
[St] Status:MEDLINE



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