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Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

ABSTRACT: Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

PROVIDER: PRJEB18611 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1758000.fastq.gz	Fastqsanger.gz
	ERR1757981.fastq.gz	Fastqsanger.gz
	ERR1757991.fastq.gz	Fastqsanger.gz
	ERR1758011.fastq.gz	Fastqsanger.gz
	ERR1758002.fastq.gz	Fastqsanger.gz

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Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

Project description:Cell activation is a vital step for T cell memory/effector differentiation as well as for productive HIV infection. To identify novel regulators of this process, we used next generation sequencing to profile changes in microRNA expression occurring in purified human naive CD4 T cells in response to TCR stimulation and HIV infection. HIV infection had no significant impact on global miR expression in quiescent nave CD4 T cells. We identified miR-34c-5p as a novel miR strongly induced by TCR stimulation of nave CD4 T cells, and found that it was consistently down-regulated in response to viral infection. Over-expression of miR-34c-5p had a positive effect on HIV-1 replication. Finally, we demonstrated that miR-34c-5p alters the expression of several genes involved in TCR signaling and cell activation, identifying it as a novel regulator of nave CD4 T cell activation potentially targeted by HIV infection.

2016-12-21 | E-MTAB-4214 | biostudies-arrayexpress

Deep sequencing of human naive CD4 T cells identifies miR-34c-5p as a novel regulator of T cell activation and HIV replication

Project description:We generated a model for miR-34c-5p overexpression by transfecting Jurkat T cell line with a pcDNA3 vector containing the pre-miR-34c-5p precursor sequence and selecting for antibiotic resistance to isolate both pools and clones of stably transfected cells (J34c cells), in parallel with control cells transfected with the empty parental vector (JÃ cells). Both pools of stably transfected cells and the derived clonal lines expressed high levels of the miR.

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Project description:In this study, treatment-naive HIV, HCV mono-/co-infected individuals with CD4+ T cell counts >300/?l were recruited and their global gene expression profiles were investigated. By gene set enrichment analysis (GSEA), we revealed that gene sets of cell cycle progression, innate immune response and some transcription factors in CD4+ T cells were affected mainly by HIV; while genes associated with extracellular matrix (ECM), Beta cell development and insulin synthesis and secretion were the major targets of HCV. For metabolic pathways, it was modulated by both viruses. Besides, for the first time, our data uncovered the importance of GPCR signaling pathway during HCV, HIV infections. These data for the first time offer genetic basis for HCV/HIV mono-/co- infections, which will facilitate the understanding of the interaction of HCV/HIV in vivo and how they subvert the human gene machinery at the individual cell type level.

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CTNNBL1 restricts HIV-1 replication

Project description:Retroviral integration is mediated by a unique enzymatic process shared by all retroviruses and retrotransposons. During integration, double-stranded linear viral DNA is inserted into the host genome in a process catalyzed by viral-encoded integrase. However, host cell defenses against HIV-1 integration are not clear. This study identifies -catenin-like protein 1 (CTNNBL1) as a potent inhibitor of HIV-1 integration via association with viral IN and its cofactor, lens epithelium-derived growth factor/p75. CTNNBL1 overexpression blocks HIV-1 integration and inhibits viral replication, whereas CTNNBL1 depletion significantly upregulates HIV-1 integration into the genome of various target cells. Further, CTNNBL1 expression is downregulated in CD4+ T cells by activation, and CTNNBL1 depletion also facilitates HIV-1 integration in resting CD4+ T cells. Thus, host cells may employ CTNNBL1 to inhibit HIV-1 integration into the genome. This finding suggests a strategy for the treatment of HIV infections.

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Next Generation Sequencing Facilitates Quantitative Analysis of HIV Elite controller, HIV ART, HIV ART-naive and healthy control Transcriptomes

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of HIV Elite controller, HIV ART, HIV ART-naive and healthy control Transcriptomes

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MicroRNAs differentially present in the plasma of HIV elite controllers

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.

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Project description:There are 19 differentially expressed microRNAs among new HIV-infected cases, old HIV-infected cases and healthy controls. Five microRNAs show trends in healthy controls, new HIV-infected cases and old HIV-infected cases, they are hsa-miR-1291, and hsa-miR-3609 with up-trends, and hsa-miR-3162-3p, hsa-miR-874-5p and hsa-miR-4258 with down-trends.

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HSF1 Activation Can Restrict HIV Replication

Project description:Host protein folding stress responses can play important roles in RNA virus replication and evolution. Intriguingly, prior work revealed a complicated interplay between the cytosolic proteostasis stress response, controlled by its master regulator heat shock factor 1 (HSF1) and human immunodeficiency virus-1 (HIV-1). We sought to isolate HSF1 transcription factor activity from proteostasis stress and elucidate the function of HSF1 in HIV-1 lifecycle in absence of cellular stress. We used chemical genetic, stress-independent control of HSF1 activity to establish whether and how HSF1 influences HIV-1 replication. Stress-independent HSF1 induction decreased both the total quantity and infectivity of HIV-1 virions. Moreover, HIV-1 was unable to escape HSF1-mediated restriction over the course of several serial passages. These results promote continued consideration of the heat shock response as a potential target for antiviral drugs.

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Next Generation Sequencing Facilitates Quantitative Analysis of HIV Elite controller, HIV ART, HIV ART-naive and healthy control Transcriptomes

Project description:A small group of HIV-1-infected individuals, termed elite controllers (ECs), display control of HIV replication in the absence of antiretroviral therapy (ART). However, the mechanisms of resistance to HIV in ECs remains largely unknown. To identify host factors specific to the ECs that might be involved in controlling HIV infection, we performed RNA-seq transcriptome analysis, and a total of 44 samples were included. The monocytes from each sample were enriched, sequenced, and subjected to comparative transcriptome analysis to screen candidate genes that might affect resistance to HIV infection. we found several candidate genes with highly divergent expression that might contribute to the different outcomes of HIV infection in ECs and non-ECs. This finding will help elucidate the mechanisms by which ECs restrict HIV replication and represents a new approach for treatment of HIV.

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MicroRNAs differentially present in the plasma of HIV elite controllers

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