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  1 / 279936 MEDLINE  
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[PMID]:25561180
[Au] Autor:Deng K; Pertea M; Rongvaux A; Wang L; Durand CM; Ghiaur G; Lai J; McHugh HL; Hao H; Zhang H; Margolick JB; Gurer C; Murphy AJ; Valenzuela DM; Yancopoulos GD; Deeks SG; Strowig T; Kumar P; Siliciano JD; Salzberg SL; Flavell RA; Shan L; Siliciano RF
[Ad] Dirección:Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA....
[Ti] Título:Broad CTL response is required to clear latent HIV-1 due to dominance of escape mutations.
[So] Fuente:Nature;517(7534):381-5, 2015 Jan 15.
[Is] ISSN:1476-4687
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:Despite antiretroviral therapy (ART), human immunodeficiency virus (HIV)-1 persists in a stable latent reservoir, primarily in resting memory CD4(+) T cells. This reservoir presents a major barrier to the cure of HIV-1 infection. To purge the reservoir, pharmacological reactivation of latent HIV-1 has been proposed and tested both in vitro and in vivo. A key remaining question is whether virus-specific immune mechanisms, including cytotoxic T lymphocytes (CTLs), can clear infected cells in ART-treated patients after latency is reversed. Here we show that there is a striking all or none pattern for CTL escape mutations in HIV-1 Gag epitopes. Unless ART is started early, the vast majority (>98%) of latent viruses carry CTL escape mutations that render infected cells insensitive to CTLs directed at common epitopes. To solve this problem, we identified CTLs that could recognize epitopes from latent HIV-1 that were unmutated in every chronically infected patient tested. Upon stimulation, these CTLs eliminated target cells infected with autologous virus derived from the latent reservoir, both in vitro and in patient-derived humanized mice. The predominance of CTL-resistant viruses in the latent reservoir poses a major challenge to viral eradication. Our results demonstrate that chronically infected patients retain a broad-spectrum viral-specific CTL response and that appropriate boosting of this response may be required for the elimination of the latent reservoir.
[Mh] Términos MeSH primario: Genes Dominantes/genética
Genes Virales/genética
VIH-1/genética
VIH-1/inmunología
Mutación/genética
Linfocitos T Citotóxicos/inmunología
Latencia del Virus/inmunología
[Mh] Términos MeSH secundario: Enfermedad Aguda/terapia
Animales
Fármacos Anti-VIH/administración & dosificación
Fármacos Anti-VIH/farmacología
Fármacos Anti-VIH/uso terapéutico
Linfocitos T CD4-Positivos/citología
Linfocitos T CD4-Positivos/inmunología
Linfocitos T CD4-Positivos/virología
Enfermedad Crónica/quimioterapia
Epítopos de Linfocito T/genética
Epítopos de Linfocito T/inmunología
Femenino
Infecciones por VIH/sangre
Infecciones por VIH/quimioterapia
Infecciones por VIH/inmunología
Infecciones por VIH/virología
VIH-1/efectos de drogas
VIH-1/crecimiento & desarrollo
Humanos
Masculino
Ratones
ARN Viral/sangre
Carga Viral/efectos de drogas
Latencia del Virus/genética
Replicación Viral/inmunología
Productos del Gen gag del Virus de la Inmunodeficiencia Humana/genética
Productos del Gen gag del Virus de la Inmunodeficiencia Humana/inmunología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Anti-HIV Agents); 0 (Epitopes, T-Lymphocyte); 0 (RNA, Viral); 0 (gag Gene Products, Human Immunodeficiency Virus)
[Em] Mes de ingreso:1502
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:150116
[St] Status:MEDLINE
[do] DOI:10.1038/nature14053


  2 / 279936 MEDLINE  
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[PMID]:25310595
[Au] Autor:Murry JP; Godoy J; Mukim A; Swann J; Bruce JW; Ahlquist P; Bosque A; Planelles V; Spina CA; Young JA
[Ad] Dirección:Nomis Center for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Rd., La Jolla, CA 92037, USA; Division of Microbiology and Immunology, Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA....
[Ti] Título:Sulfonation pathway inhibitors block reactivation of latent HIV-1.
[So] Fuente:Virology;471-473:1-12, 2014 Dec.
[Is] ISSN:1096-0341
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Long-lived pools of latently infected cells are a significant barrier to the development of a cure for HIV-1 infection. A better understanding of the mechanisms of reactivation from latency is needed to facilitate the development of novel therapies that address this problem. Here we show that chemical inhibitors of the sulfonation pathway prevent virus reactivation, both in latently infected J-Lat and U1 cell lines and in a primary human CD4+ T cell model of latency. In each of these models, sulfonation inhibitors decreased transcription initiation from the HIV-1 promoter. These inhibitors block transcription initiation at a step that lies downstream of nucleosome remodeling and affects RNA polymerase II recruitment to the viral promoter. These results suggest that the sulfonation pathway acts by a novel mechanism to regulate efficient virus transcription initiation during reactivation from latency, and further that augmentation of this pathway could be therapeutically useful.
[Mh] Términos MeSH primario: Fármacos Anti-VIH/farmacología
Cloratos/farmacología
Guayacol/farmacología
VIH-1/efectos de drogas
Activación Viral/efectos de drogas
[Mh] Términos MeSH secundario: Fármacos Anti-VIH/administración & dosificación
Linfocitos T CD4-Positivos/virología
Línea Celular
Cloratos/administración & dosificación
Quimioterapia Combinada
Regulación Viral de la Expresión Génica/fisiología
Guayacol/administración & dosificación
Duplicado del Terminal Largo de VIH
VIH-1/metabolismo
Humanos
FN-kappa B/genética
FN-kappa B/metabolismo
ARN Polimerasa II/metabolismo
Ácidos Sulfónicos/antagonistas & inhibidores
Ácidos Sulfónicos/metabolismo
Factor de Necrosis Tumoral alfa/genética
Factor de Necrosis Tumoral alfa/metabolismo
Latencia del Virus/fisiología
[Pt] Tipo de publicación: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] Nombre de substancia:
0 (Anti-HIV Agents); 0 (Chlorates); 0 (NF-kappa B); 0 (Sulfonic Acids); 0 (Tumor Necrosis Factor-alpha); 6JKA7MAH9C (Guaiacol); EC 2.7.7.- (RNA Polymerase II)
[Em] Mes de ingreso:1502
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:141203
[St] Status:MEDLINE


  3 / 279936 MEDLINE  
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[PMID]:25253353
[Au] Autor:Soriano-Sarabia N; Bateson RE; Dahl NP; Crooks AM; Kuruc JD; Margolis DM; Archin NM
[Ad] Dirección:Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA....
[Ti] Título:Quantitation of replication-competent HIV-1 in populations of resting CD4+ T cells.
[So] Fuente:J Virol;88(24):14070-7, 2014 Dec.
[Is] ISSN:1098-5514
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:UNLABELLED: Central memory (TCM) CD4(+) T cells are the principal reservoir of latent HIV-1 infection that persists despite durable, successful antiretroviral therapy (ART). In a study that measured HIV DNA in 17 patients and replication-competent HIV in 4 patients, pools of resting and activated transitional memory (T(TM)) CD4(+) T cells were found to be a reservoir for HIV infection. As defective viruses account for the majority of integrated HIV DNA and do not reflect the actual frequency of latent, replication-competent proviral infection, we assessed the specific contribution of resting T(TM) cells to latent HIV infection. We measured the frequency of replication-competent HIV in purified resting memory cell subpopulations by a limiting-dilution, quantitative viral outgrowth assay (QVOA). HIV was routinely detected within the resting central memory compartment but was infrequently detected within the resting T(TM) compartment. These observations suggest that prolonged ART may limit persistent latent infection in the T(TM) compartment. Our results confirm the importance of latent infection within the TCM compartment and again focus attention on these cells as the most important latent viral reservoir. While proliferation may drive expansion of detectable viral genomes in cells, the frequency of replication-competent HIV must be carefully assessed. Latent infection appears to wane within the transitional memory compartment in patients who have sustained successful viral suppression via ART or were treated very early in infection. IMPORTANCE: Antiretroviral therapy (ART) has led to a significant decrease in morbidity and mortality among HIV-infected patients. However, HIV integrates into the genome of CD4(+) T cells, generating pools of long-lived cells that are reservoirs of latent HIV. Two main subsets of CD4(+) T cells, central memory and transitional memory cells, were reported to be major reservoirs of HIV infection. However, this study primarily measured the HIV DNA content, which also includes defective proviruses that would not be able to replicate and initiate new rounds of infection. By analyzing the replication-competent virus in both cell subsets, we showed that transitional memory cells may not be a durable reservoir in patients on successful ART.
[Mh] Términos MeSH primario: Linfocitos T CD4-Positivos/virología
VIH-1/aislamiento & purificación
VIH-1/fisiología
Carga Viral
Replicación Viral
[Mh] Términos MeSH secundario: Adulto
Humanos
Masculino
Mediana Edad
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mes de ingreso:1501
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:141122
[St] Status:MEDLINE
[do] DOI:10.1128/JVI.01900-14


  4 / 279936 MEDLINE  
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[PMID]:25402363
[Au] Autor:Archin NM; Sung JM; Garrido C; Soriano-Sarabia N; Margolis DM
[Ad] Dirección:Department of Medicine, University of North Carolina at Chapel Hill....
[Ti] Título:Eradicating HIV-1 infection: seeking to clear a persistent pathogen.
[So] Fuente:Nat Rev Microbiol;12(11):750-64, 2014 Nov.
[Is] ISSN:1740-1534
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:Effective antiretroviral therapy (ART) blunts viraemia, which enables HIV-1-infected individuals to control infection and live long, productive lives. However, HIV-1 infection remains incurable owing to the persistence of a viral reservoir that harbours integrated provirus within host cellular DNA. This latent infection is unaffected by ART and hidden from the immune system. Recent studies have focused on the development of therapies to disrupt latency. These efforts unmasked residual viral genomes and highlighted the need to enable the clearance of latently infected cells, perhaps via old and new strategies that improve the HIV-1-specific immune response. In this Review, we explore new approaches to eradicate established HIV-1 infection and avoid the burden of lifelong ART.
[Mh] Términos MeSH primario: Fármacos Anti-VIH/uso terapéutico
Erradicación de la Enfermedad/métodos
Infecciones por VIH/prevención & control
VIH-1/fisiología
Latencia del Virus/fisiología
[Mh] Términos MeSH secundario: Animales
Línea Celular
Modelos Animales de Enfermedad
Infecciones por VIH/inmunología
Infecciones por VIH/terapia
Infecciones por VIH/virología
Humanos
Viremia
Integración Viral
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nombre de substancia:
0 (Anti-HIV Agents)
[Em] Mes de ingreso:1501
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:141118
[St] Status:MEDLINE
[do] DOI:10.1038/nrmicro3352


  5 / 279936 MEDLINE  
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[PMID]:25140907
[Au] Autor:Chung MH; Beck IA; Dross S; Tapia K; Kiarie JN; Richardson BA; Overbaugh J; Sakr SR; John-Stewart GC; Frenkel LM
[Ad] Dirección:Departments of *Global Health; †Medicine; ‡Epidemiology, University of Washington, Seattle, WA; §Center for Global Infectious Disease Research, Seattle Children's Research Institute, Seattle, WA; ‖Department of Obstetrics and Gynaecology, University of Nairobi, Nairobi, Kenya; ¶Department of Biostatistics, University of Washington, Seattle, WA; #Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA; **Division of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA; ††Coptic Hospital, Nairobi, Kenya; Departments of ‡‡Pediatrics; and §§Laboratory Medicine, University of Washington, Seattle, WA.
[Ti] Título:Oligonucleotide ligation assay detects HIV drug resistance associated with virologic failure among antiretroviral-naive adults in Kenya.
[So] Fuente:J Acquir Immune Defic Syndr;67(3):246-53, 2014 Nov 1.
[Is] ISSN:1944-7884
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Transmitted drug resistance (TDR) is increasing in some areas of Africa. Detection of TDR may predict virologic failure of first-line nonnucleoside reverse transcriptase inhibitor (NNRTI)-based antiretroviral therapy (ART). We evaluated the utility of a relatively inexpensive oligonucleotide ligation assay (OLA) to detect clinically relevant TDR at the time of ART initiation. METHODS: Pre-ART plasmas from ART-naive Kenyans initiating an NNRTI-based fixed-dose combination ART in a randomized adherence trial conducted in 2006 were retrospectively analyzed by OLA for mutations conferring resistance to NNRTI (K103N, Y181C, and G190A) and lamivudine (M184V). Post-ART plasmas were analyzed for virologic failure (≥1000 copies/mL) at 6-month intervals over 18-month follow-up. Pre-ART plasmas of those with virologic failure were evaluated for drug resistance by consensus and 454-pyrosequencing. RESULTS: Among 386 participants, TDR was detected by OLA in 3.89% (95% confidence interval: 2.19 to 6.33) and was associated with a 10-fold higher rate of virologic failure (hazard ratio: 10.39; 95% confidence interval: 3.23 to 32.41; P < 0.001) compared with those without TDR. OLA detected 24 TDR mutations (K103N: n = 13; Y181C: n = 5; G190A: n = 3; M184V: n = 3) in 15 subjects (NNRTI: n = 15; 3TC: n = 3). Among 51 participants who developed virologic failure, consensus sequencing did not detect additional TDR mutations conferring high-level resistance, and pyrosequencing only detected additional mutations at frequencies <2%. Mutant frequencies <2% at ART initiation were significantly less likely to be found at the time of virologic failure compared with frequencies ≥2% (22% vs. 63%; P < 0.001). CONCLUSIONS: Detection of TDR by a point mutation assay may prevent the use of suboptimal ART.
[Mh] Términos MeSH primario: Fármacos Anti-VIH/uso terapéutico
Terapia Antirretroviral Altamente Activa
Farmacorresistencia Viral
Infecciones por VIH/quimioterapia
VIH-1/efectos de drogas
Técnicas de Diagnóstico Molecular/métodos
Inhibidores de Transcriptasa Inversa/uso terapéutico
[Mh] Términos MeSH secundario: Adulto
ADN Viral/análisis
Femenino
Infecciones por VIH/virología
VIH-1/genética
VIH-1/aislamiento & purificación
Humanos
Kenia
Reacción en Cadena de la Ligasa/métodos
Masculino
Mediana Edad
Mutación
Sondas de Oligonucleótidos/uso diagnóstico
Sondas de Oligonucleótidos/genética
Estudios Retrospectivos
Insuficiencia del Tratamiento
Carga Viral
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, AMERICAN RECOVERY AND REINVESTMENT ACT; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nombre de substancia:
0 (Anti-HIV Agents); 0 (DNA, Viral); 0 (Oligonucleotide Probes); 0 (Reverse Transcriptase Inhibitors)
[Em] Mes de ingreso:1412
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM; X
[Da] Fecha de ingreso para procesamiento:141014
[St] Status:MEDLINE
[do] DOI:10.1097/QAI.0000000000000312


  6 / 279936 MEDLINE  
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[PMID]:24924152
[Au] Autor:Jenabian MA; Patel M; Kema I; Vyboh K; Kanagaratham C; Radzioch D; Thébault P; Lapointe R; Gilmore N; Ancuta P; Tremblay C; Routy JP
[Ad] Dirección:Chronic Viral Illness Service, McGill University Health Centre, Montreal, QC, Canada; Research Institute, McGill University Health Centre, Montreal, QC, Canada.
[Ti] Título:Soluble CD40-ligand (sCD40L, sCD154) plays an immunosuppressive role via regulatory T cell expansion in HIV infection.
[So] Fuente:Clin Exp Immunol;178(1):102-11, 2014 Oct.
[Is] ISSN:1365-2249
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:CD40/CD40-ligand (CD40L) signalling is a key stimulatory pathway which triggers the tryptophan (Trp) catabolizing enzyme IDO in dendritic cells and is immunosuppressive in cancer. We reported IDO-induced Trp catabolism results in a T helper type 17 (Th17)/regulatory T cell (Treg ) imbalance, and favours microbial translocation in HIV chronic infection. Here we assessed the link between sCD40L, Tregs and IDO activity in HIV-infected patients with different clinical outcomes. Plasmatic sCD40L and inflammatory cytokines were assessed in anti-retroviral therapy (ART)-naive, ART-successfully treated (ST), elite controllers (EC) and healthy subjects (HS). Plasma levels of Trp and its metabolite Kynurenine (Kyn) were measured by isotope dilution tandem mass spectrometry and sCD14 was assessed by enzyme-linked immunosorbent assay (ELISA). IDO-mRNA expression was quantified by reverse transcription-polymerase chain reaction (RT-PCR). The in-vitro functional assay of sCD40L on Treg induction and T cell activation were assessed on peripheral blood mononuclear cells (PBMCs) from HS. sCD40L levels in ART-naive subjects were significantly higher compared to ST and HS, whereas EC showed only a minor increase. In ART-naive alone, sCD40L was correlated with T cell activation, IDO-mRNA expression and CD4 T cell depletion but not with viral load. sCD40L was correlated positively with IDO enzymatic activity (Kyn/Trp ratio), Treg frequency, plasma sCD14 and inflammatory soluble factors in all HIV-infected patients. In-vitro functional sCD40L stimulation induced Treg expansion and favoured Treg differentiation by reducing central memory and increasing terminal effector Treg proportion. sCD40L also increased T cell activation measured by co-expression of CD38/human leucocyte antigen D-related (HLA-DR). These results indicate that elevated sCD40L induces immunosuppression in HIV infection by mediating IDO-induced Trp catabolism and Treg expansion.
[Mh] Términos MeSH primario: Ligando de CD40/inmunología
Infecciones por VIH/inmunología
Inmunosupresores/inmunología
Linfocitos T Reguladores/inmunología
[Mh] Términos MeSH secundario: Adulto
Linfocitos T CD4-Positivos/inmunología
Femenino
Humanos
Tolerancia Inmunológica
Quinurenina/inmunología
Leucocitos Mononucleares/inmunología
Activación de Linfocitos/inmunología
Masculino
Mediana Edad
Triptófano/inmunología
Adulto Joven
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Immunosuppressive Agents); 147205-72-9 (CD40 Ligand); 343-65-7 (Kynurenine); 8DUH1N11BX (Tryptophan)
[Em] Mes de ingreso:1412
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140908
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12396


  7 / 279936 MEDLINE  
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[PMID]:24853045
[Au] Autor:Lohman-Payne B; Sandifer T; OhAinle M; Crudder C; Lynch J; Omenda MM; Maroa J; Fowke K; John-Stewart GC; Farquhar C
[Ad] Dirección:Department of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya; Department of Medicine, University of Washington, Seattle, Washington, USA; Department of Global Health, University of Washington, Seattle, Washington, USA.
[Ti] Título:In-utero infection with HIV-1 associated with suppressed lymphoproliferative responses at birth.
[So] Fuente:Clin Exp Immunol;178(1):86-93, 2014 Oct.
[Is] ISSN:1365-2249
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:In-utero exposure to HIV-1 may affect the immune system of the developing child and may induce HIV-1-specific immune responses, even in the absence of HIV-1 infection. We evaluated lymphoproliferative capacity at birth among 40 HIV-1-uninfected infants born to HIV-1-infected mothers and 10 infants who had acquired HIV-1 in utero. Cord blood mononuclear cells were assayed using [(3) H]-thymidine incorporation for proliferation in response to HIV-1 p55-gag and the control stimuli phytohaemagglutinin (PHA), Staphylococcus enterotoxin B (SEB) and allogeneic cells. In response to HIV-1 p55-gag, eight (20%) HIV-1-exposed, uninfected (EU) infants had a stimulation index (SI) ≥ 2 and three (30%) in-utero HIV-1 infected infants had SI ≥2. The frequency and magnitude of responses to HIV-1 p55-gag were low overall, and did not differ statistically between groups. However, proliferative responses to control stimuli were significantly higher in EU infants than in infants infected in utero, with a median SI in response to PHA of 123 [interquartile range (IQR) 77-231] versus 18 (IQR 4-86) between EU and infected infants, respectively (P < 0·001). Among infected infants, gestational maturity was associated with the strength of HIV-1 p55-gag response (P < 0·001); neither maternal nor infant HIV-1 viral load was associated. In summary, EU and HIV-1-infected infants mounted HIV-1-specific lymphoproliferative responses at similar rates (20-30%), and although global immune function was preserved among EU infants, neonatal immune responses were significantly compromised by HIV-1 infection. Such early lymphoproliferative compromise may, in part, explain rapid progression to AIDS and death among HIV-1-infected infants.
[Mh] Términos MeSH primario: Infecciones por VIH/inmunología
VIH-1/inmunología
Complicaciones Infecciosas del Embarazo/inmunología
[Mh] Términos MeSH secundario: Síndrome de Inmunodeficiencia Adquirida/inmunología
Síndrome de Inmunodeficiencia Adquirida/virología
Adulto
Proliferación de la Célula
Femenino
Sangre Fetal/inmunología
Sangre Fetal/virología
Infecciones por VIH/virología
Humanos
Lactante
Transmisión Vertical de Enfermedad Infecciosa
Activación de Linfocitos/inmunología
Embarazo
Complicaciones Infecciosas del Embarazo/virología
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mes de ingreso:1412
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140908
[St] Status:MEDLINE
[do] DOI:10.1111/cei.12386


  8 / 279936 MEDLINE  
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[PMID]:24962285
[Au] Autor:Milloy MJ; Montaner JS; Wood E
[Ad] Dirección:British Columbia Centre for Excellence in HIV/AIDS, 608-1081 Burrard Street, Vancouver, BC, V6Z 1Y6, Canada, mjmilloy@cfenet.ubc.ca.
[Ti] Título:Incarceration of people living with HIV/AIDS: implications for treatment-as-prevention.
[So] Fuente:Curr HIV/AIDS Rep;11(3):308-16, 2014 Sep.
[Is] ISSN:1548-3576
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Contact with the criminal justice system, including incarceration, is a common experience for many people living with HIV/AIDS. Optimism has recently been expressed that correctional facilities could be important locations for treatment-as-prevention (TasP)-based initiatives. We review recent findings regarding the effect of incarceration on patterns of HIV transmission, testing, treatment initiation and retention. We found that the prevalence of HIV infection among incarcerated individuals remains higher than analogous non-incarcerated populations. Recent studies have shown that voluntary HIV/AIDS testing is feasible in many correctional facilities, although the number of previously undiagnosed individuals identified has been modest. Studies have implied enhanced linkage to HIV/AIDS treatment and care in jails in the United States was associated with improvements in the HIV cascade of care. However, for many individuals living with HIV/AIDS, exposure to the correctional system remains an important barrier to retention in HIV/AIDS treatment and care. Future research should evaluate structural interventions to address these barriers and facilitate the scale-up of TasP-based efforts among individuals living in correctional settings.
[Mh] Términos MeSH primario: Síndrome de Inmunodeficiencia Adquirida/prevención & control
Fármacos Anti-VIH/uso terapéutico
Infecciones por VIH/prevención & control
Prisioneros
[Mh] Términos MeSH secundario: Síndrome de Inmunodeficiencia Adquirida/diagnóstico
Síndrome de Inmunodeficiencia Adquirida/quimioterapia
Síndrome de Inmunodeficiencia Adquirida/transmisión
Fármacos Anti-VIH/administración & dosificación
Infecciones por VIH/diagnóstico
Infecciones por VIH/quimioterapia
Infecciones por VIH/transmisión
Humanos
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Anti-HIV Agents)
[Em] Mes de ingreso:1502
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:140805
[St] Status:MEDLINE
[do] DOI:10.1007/s11904-014-0214-z


  9 / 279936 MEDLINE  
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[PMID]:24752082
[Au] Autor:Gasper MA; Kunwar P; Itaya G; Lejarcegui N; Bosire R; Maleche-Obimbo E; Wamalwa D; Slyker J; Overbaugh J; Horton H; Sodora DL; John-Stewart G; Lohman-Payne B
[Ad] Dirección:aSeattle Biomedical Research Institute bDepartment of Global Health cDepartment of Medicine dDepartment of Epidemiology eDepartment of Pediatrics, University of Washington fFred Hutchinson Cancer Research Center, Seattle, Washington, USA gCenter for Public Health Research, Kenya Medical Research Institute hDepartment of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya.
[Ti] Título:Natural killer cell and T-cell subset distributions and activation influence susceptibility to perinatal HIV-1 infection.
[So] Fuente:AIDS;28(8):1115-24, 2014 May 15.
[Is] ISSN:1473-5571
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:OBJECTIVE: To determine neonatal immunologic factors that correlate with mother-to-child-transmission of HIV-1. DESIGN: This case-control study compared cord blood natural killer (NK) and T-cell populations of HIV-1 exposed infants who subsequently acquired infection by 1 month (cases) to those who remained uninfected by 1 year of life (controls). Control specimens were selected by proportional match on maternal viral load. METHODS: Cryopreserved cord blood mononuclear cells (CBMCs) were thawed and stained for multiparameter flow cytometry to detect NK and T-cell subsets and activation status. CBMCs were also used in a viral suppression assay to evaluate NK cell inhibition of HIV-1 replication in autologous CD4 T cells. RESULTS: Cord blood from cases contained a skewed NK cell repertoire characterized by an increased proportion of CD16CD56 NK cells. In addition, cases displayed less-activated CD16CD56 NK cells and CD8 T cells, based on HLA-DRCD38 costaining. NK cell suppression of HIV-1 replication ex vivo correlated with the proportion of acutely activated CD68CD16CD56 NK cells. Finally, we detected a higher proportion of CD27CD45RA effector memory CD4 and CD8 T cells in cord blood from cases compared with controls. CONCLUSION: When controlled for maternal viral load, cord blood from infants who acquired HIV-1 had a higher proportion of CD16CD56 NK cells, lower NK cell activation and higher levels of mature T cells (potential HIV-1 targets) than control infants who remained uninfected. Our data provide evidence that infant HIV-1 acquisition may be influenced by both innate and adaptive immune cell phenotypes and activation status.
[Mh] Términos MeSH primario: Susceptibilidad a Enfermedades/inmunología
Infecciones por VIH/inmunología
VIH-1/inmunología
Transmisión Vertical de Enfermedad Infecciosa
Células Asesinas Naturales/metabolismo
Subgrupos de Linfocitos T/metabolismo
[Mh] Términos MeSH secundario: Adulto
Estudios de Casos y Controles
Femenino
Sangre Fetal/inmunología
Sangre Fetal/metabolismo
Infecciones por VIH/metabolismo
Humanos
Lactante
Recién Nacido
Embarazo
Carga Viral
Adulto Joven
[Pt] Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mes de ingreso:1502
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM; X
[Da] Fecha de ingreso para procesamiento:140717
[St] Status:MEDLINE
[do] DOI:10.1097/QAD.0000000000000263


  10 / 279936 MEDLINE  
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[PMID]:24785950
[Au] Autor:Kidzeru EB; Hesseling AC; Passmore JA; Myer L; Gamieldien H; Tchakoute CT; Gray CM; Sodora DL; Jaspan HB
[Ad] Dirección:aDivision of Immunology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town bDesmond Tutu TB Centre, Faculty of Medicine and Health Sciences, Stellenbosch University, Parow cDivision of Virology, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town dNational Health Laboratory Services, South Africa eDivision of Epidemiology & Biostatistics, School of Public Health & Family Medicine, University of Cape Town, Cape Town, South Africa fSeattle Biomedical Research Institute, Seattle, Washington, USA.
[Ti] Título:In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants.
[So] Fuente:AIDS;28(10):1421-30, 2014 Jun 19.
[Is] ISSN:1473-5571
[Cp] País de publicación:England
[La] Idioma:eng
[Ab] Resumen:OBJECTIVE: In sub-Saharan Africa, HIV-exposed uninfected (HEU) infants have higher morbidity and mortality than HIV-unexposed infants. To evaluate whether immune dysfunction contributes to this vulnerability of HEU infants, we conducted a longitudinal, observational cohort study to assess T-cell immune responses to infant vaccines (Mycobacterium bovis BCG and acellular pertussis) and staphylococcal enterotoxin B (SEB). In total, 46 HEU and 46 HIV-unexposed infants were recruited from Khayelitsha, Cape Town. METHODS: Vaccine-specific T-cell proliferation (Ki67 expression) and intracellular expression of four cytokines [interferon-γ, interleukin (IL)-2, IL-13 and IL-17] were measured after whole blood stimulation with antigens at 6 and 14 weeks of age. RESULTS: HEU infants demonstrated elevated BCG-specific CD4 and CD8 T-cell proliferative responses at 14 weeks (P  = 0.041 and 0.002, respectively). These responses were significantly increased even after adjusting for birth weight, feeding mode and gestational age. Similar to BCG, increased CD4 and CD8 T-cell proliferation was evident in response to SEB stimulation (P  = 0.004 and 0.002, respectively), although pertussis-specific T cells proliferated comparably between the two groups. Within HEU infants, maternal CD4 cell count and length of antenatal antiretroviral exposure had no effect on T-cell proliferation to BCG or SEB. HIV exposure significantly diminished measurable cytokine polyfunctionality in response to BCG, Bordetella pertussis and SEB stimulation. CONCLUSION: These data show for the first time, when adjusting for confounders, that exposure to HIV in utero is associated with significant alterations to CD4 and CD8T-cell immune responses in infants to vaccines and nonspecific antigens.
[Mh] Términos MeSH primario: Vacuna BCG/inmunología
Infecciones por VIH/inmunología
Intercambio Materno-Fetal/inmunología
Vacuna contra la Tos Ferina/inmunología
Complicaciones Infecciosas del Embarazo/inmunología
Vacunas Estafilocócicas/inmunología
Linfocitos T/inmunología
[Mh] Términos MeSH secundario: África del Sur del Sahara
Vacuna BCG/administración & dosificación
Proliferación de la Célula
Estudios de Cohortes
Citocinas/biosíntesis
Femenino
Humanos
Lactante
Recién Nacido
Antígeno Ki-67/análisis
Estudios Longitudinales
Masculino
Vacuna contra la Tos Ferina/administración & dosificación
Embarazo
Vacunas Estafilocócicas/administración & dosificación
Vacunas Acelulares/administración & dosificación
Vacunas Acelulares/inmunología
[Pt] Tipo de publicación:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (BCG Vaccine); 0 (Cytokines); 0 (Ki-67 Antigen); 0 (Pertussis Vaccine); 0 (Staphylococcal Vaccines); 0 (Vaccines, Acellular)
[Em] Mes de ingreso:1501
[Cu] Fecha actualización por clase:150321
[Lr] Fecha última revisión:150321
[Sb] Subgrupo de revista:IM; X
[Da] Fecha de ingreso para procesamiento:140606
[St] Status:MEDLINE
[do] DOI:10.1097/QAD.0000000000000292



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