Expression analysis of microRNAs in plasma of new HIV-infected cases, old HIV-infected cases and healthy controls.
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ABSTRACT:
ORGANISM(S): Mus musculus Rattus norvegicus Homo sapiens
PROVIDER: GSE103555 | GEO | 2017/12/01
SECONDARY ACCESSION(S): PRJNA401865
REPOSITORIES: GEO
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Project description:Elite controllers maintain HIV-1 viral loads below the limit of detection. The mechanisms responsible for this phenomenon are poorly understood. As microRNAs (miRNAs) are regulators of gene expression and some of them modulate HIV infection, we have studied the miRNA profile in plasma from HIV elite controllers and chronically infected individuals and compared against healthy donors. Several miRNAs correlate with CD4+ T cell count or with the known time of infection. No significant differences were observed between elite controllers and healthy donors; however, 16 miRNAs were different in the plasma of chronic infected versus healthy donors. In addition, levels of hsa-miR-29b-3p, hsa-miR-33a-5p and hsa-miR-146a-5p were higher in plasma from elite controllers than chronic infected and hsa-miR-29b-3p and hsa-miR-33a-5p overexpression significantly reduced the viral production in MT2 cells. Therefore, levels of circulating miRNAs might be of diagnostic and/or prognostic value for HIV infection. Additionally, hsa-miR-29b-3p and miR-33a-5p may be used in therapeutic strategies.
2014-08-04 | GSE58868 | GEO
Project description:Elite controllers maintain HIV-1 viral loads below the limit of detection. The mechanisms responsible for this phenomenon are poorly understood. As microRNAs (miRNAs) are regulators of gene expression and some of them modulate HIV infection, we have studied the miRNA profile in plasma from HIV elite controllers and chronically infected individuals and compared against healthy donors. Several miRNAs correlate with CD4+ T cell count or with the known time of infection. No significant differences were observed between elite controllers and healthy donors; however, 16 miRNAs were different in the plasma of chronic infected versus healthy donors. In addition, levels of hsa-miR-29b-3p, hsa-miR-33a-5p and hsa-miR-146a-5p were higher in plasma from elite controllers than chronic infected and hsa-miR-29b-3p and hsa-miR-33a-5p overexpression significantly reduced the viral production in MT2 cells. Therefore, levels of circulating miRNAs might be of diagnostic and/or prognostic value for HIV infection. Additionally, hsa-miR-29b-3p and miR-33a-5p may be used in therapeutic strategies. An exploratory cross-sectional study of microRNA levels in EDTA plasma samples. Plasma samples were obtained from 24 subjects and were classified in 3 groups, 9 Elite Controllers (defined as individuals with plasma viral load (PVL) < 50 copies/ml, CD4 count >350/ml), 9 chronic HIV patients (CH) under anti-retroviral treatment and 6 healthy HIV negative donors (HD). This study was approved by the HuM-CM-)sped Foundation Ethics Committee and informed consent was obtained from all subjects.
2014-08-04 | E-GEOD-58868 | biostudies-arrayexpress
Project description:Herein expression trends of host miRNA were measured in HIV-1 latently infected and persistent replication cells, as well as the control cells. HIV-1 latency infection was established by infecting CEM-SS lymphocytes with HIV-1 Bru strain. After selection and long-term culture, the chronically infected cell showed the characteristics of latency definition: 1. The provirus was intergrated in to the host genome.2. No viral expression could be detected during culture.3 .Cell stimulators, such as TNFa,PMA, etc, reactivate the viral expression. As expected, miRNA trend was different in HIV-1 latency when compared to the control or HIV-1 replication. A subset of miRNAs is enriched in HIV-1 latency model. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate HIV-1 infection mode.
2012-12-01 | GSE38388 | GEO
Project description:Herein expression trends of host miRNA were measured in HIV-1 latently infected and persistent replication cells, as well as the control cells. HIV-1 latency infection was established by infecting CEM-SS lymphocytes with HIV-1 Bru strain. After selection and long-term culture, the chronically infected cell showed the characteristics of latency definition: 1. The provirus was intergrated in to the host genome.2. No viral expression could be detected during culture.3 .Cell stimulators, such as TNFa,PMA, etc, reactivate the viral expression. As expected, miRNA trend was different in HIV-1 latency when compared to the control or HIV-1 replication. A subset of miRNAs is enriched in HIV-1 latency model. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate HIV-1 infection mode. In this study, the in vitro steady cell culture was used to explore the miRNA transcription signatures in HIV-1 infection. miRNA profiles were performed and compared among normal control,HIV-1 latency and HIV-1 replication .
2012-12-01 | E-GEOD-38388 | biostudies-arrayexpress
Project description:Objective: To elucidate molecular mechanisms of neurocognitive dysfunction in long-term HIV-infected individuals by assessing the microRNA (miR) profile and determining clinical and neurocognitive correlates to miR expression. Design: Analysis of miR profile in frontal cortex of retrospectively-identified autopsy cases of longitudinally-followed subjects with HIV-infection and age/sex-matched controls. HIV-subjects had semi-annual neuropsychiatric and clinical testing, at autopsy, tissue was archived. Methods: MiR repertoires were profiled from frontal cortices. Analysis of variance (ANOVA) and Tukey Honestly Sigificant Difference (HSD) tests with Benjamini-Hochberg correction for multiple comparisons were used to compare expression among the three groups. Pairwise correlations were used to identify neuropsychiatric variable that correlatee with expression of miRs. Results: MiRs were significantly different by HIV-status: miR-103, miR-125a, miR-380, miR-422a, miR-515, miR-520b, miR0618, miR-886, and miR-9. Many miRs correlated with neuropsychiatric outcomes like Learning, Memory, Executive, Verbal, and Motor deficit scores. Conclusions: MiRs are clearly dysregulated in the frontal cortex of HIV-positive individuals. Only a few miRs were significantly dysregulated in only the methamphetamine group. Our study identifies miRs that form rational targets for further inquiry on biochemical mechanisms of HIV-related neurocognitive deficits. Learning deficit score correlates with expression of more miRs than other parameters.
2013-01-01 | GSE41952 | GEO
Project description:Using HIV-1 SortSeq, we identified HIV-1-infected cells containing inducible HIV-1 for RNAseq from resting CD4+ T cells treated with PMA/ionomycin for 16 hours from HIV-1-infected, antiretroviral therapy treated, virally suppressed individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.
2020-05-15 | GSE126230 | GEO
Project description:Objective: To elucidate molecular mechanisms of neurocognitive dysfunction in long-term HIV-infected individuals by assessing the microRNA (miR) profile and determining clinical and neurocognitive correlates to miR expression. Design: Analysis of miR profile in frontal cortex of retrospectively-identified autopsy cases of longitudinally-followed subjects with HIV-infection and age/sex-matched controls. HIV-subjects had semi-annual neuropsychiatric and clinical testing, at autopsy, tissue was archived. Methods: MiR repertoires were profiled from frontal cortices. Analysis of variance (ANOVA) and Tukey Honestly Sigificant Difference (HSD) tests with Benjamini-Hochberg correction for multiple comparisons were used to compare expression among the three groups. Pairwise correlations were used to identify neuropsychiatric variable that correlatee with expression of miRs. Results: MiRs were significantly different by HIV-status: miR-103, miR-125a, miR-380, miR-422a, miR-515, miR-520b, miR0618, miR-886, and miR-9. Many miRs correlated with neuropsychiatric outcomes like Learning, Memory, Executive, Verbal, and Motor deficit scores. Conclusions: MiRs are clearly dysregulated in the frontal cortex of HIV-positive individuals. Only a few miRs were significantly dysregulated in only the methamphetamine group. Our study identifies miRs that form rational targets for further inquiry on biochemical mechanisms of HIV-related neurocognitive deficits. Learning deficit score correlates with expression of more miRs than other parameters. A total of 11 HIV positive individuals were analyzed, 5 of which had a past history of methamphetamine ABUSE, and 5 age-matched HIV-negative normal Controls. Technical duplicates are included. Included are clinical and neuropsychiatric data from most recent visit before time of death. This is a retrospective autopsy study of longitudinally-followed subjects on miRNA levels in the frontal cortex.
2013-01-01 | E-GEOD-41952 | biostudies-arrayexpress
Project description:Background: The emerging relationship between microRNAs (miRNA) and viral-control is a topic of interest in the field of HIV. Host-genome might play an important role in the control of viremia. The aim of this study was to assess the specific miRNA profile that could contribute to the control of HIV replication in Elite Controllers. Results: After adequate normalization, expression profile of 286 human miRNAs (hsa-miR) was evaluated in 29 individuals classified in 4 groups: 8 elite controllers (EC; viral load <50 cp/ml without treatment), 8 viremic progressors (VP; VL>5000 cp/ml without treatment), 8 patients under antiretroviral treatment (ART; VL<200cp/ml) and 5 uninfected individuals (HIV-) through TaqMan® Array Human microRNA Cards v3.0. A differential expression pattern consisting of 23 miRNAs overcame significantly different when comparing EC and VP. Profiling analysis segregated the population in two different blocks: while EC and HIV- clustered together in the same block (EC/HIV-_block 1), VP and ART individuals clustered together in a second block (VP/ART_block 2). Two inversely expressed miRNA patterns were determined within those two blocks: a set of 4 miRNAs (hsa-miR-221, -27a, -27b and -29b) was up-expressed in EC/HIV-_block and down-expressed in VP/ART_block while 19 miRNAs were down-expressed in block 1 and up-expressed in block 2. Differential miRNAs were successfully validated through individual RT-qPCR assays. Conclusions: Profile in EC resembled HIV- and differentially clusters with VP and ART. Therefore, differential clustering does not rely on undetectable viremia. Peripheral blood mononuclear cell samples were from five uninfected controls, eight viremic HIV-1-infected patients, eight HIV-1 elite controllers with undetectable viral load and eight HIV-1antiretroviral treated individuals with undetectable viral load.
2014-05-06 | E-GEOD-57323 | biostudies-arrayexpress
Project description:HIV-1 SortSeq identifies HIV-1-infected cells from HIV-1-infected individuals
| PRJNA521359 | ENA
Project description:Herein expression trends of host miRNA were measured in CEMx174 lymphocytes infected with HIV-1NL4-3 or derivative strains deficient in Tat RSS activity (RSS) or vif-/vpr (VV), or unexposed to virus. As expected from previous studies, miRNA trends were different in naive and HIV-1 infected cells. Moreover, miRNA expression trends were similar for HIV-1 and vif-/vpr-deficient HIV-1, but diverged for RSS. Rather than generalized changes in miRNA levels, HIV-1 bearing the Tat K51A RSS mutation changed the steady state of a subset of miRNAs. The results are attributable to reduction in miRNA stability or change in miRNAs activity that altered steady state expression. Comparison of the miRNA expression trends in patient PBMC and the CEMx174 lymphocytes determined >50% overlap with a subset of miRNAs identified in patients, supporting the utility of HIV-1 cell culture model to refine experimental design with patient samples, which represent miRNA profiles of co-isolated infected and uninfected cells. Our results indicate that ablation of Tat RNA silencing suppressor activity in HIV-1 changes the steady state of a subset of host mature miRNA. The observation reinforces the concept of active HIV-1 interplay with host small RNAs that modulate replication and spread. The study validated the utility of derivative HIV-1 strains to explore the interface of viral genes with host small RNA activity. In this study the microRNA profiles of CEMx174 cells infected with HIV-1 NL4-3 or derivative viruses deficient in Vif/Vpr or Tat RNA silencing suppressor activity were compared to mock infected cells. The samples were analyzed in duplicate.
2011-03-01 | E-GEOD-21892 | biostudies-arrayexpress