Ontology highlight
ABSTRACT:
PROVIDER: PRJNA318913 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3403080.fastq.gz | Fastqsanger.gz | |||
| SRR3403090.fastq.gz | Fastqsanger.gz | |||
| SRR3403100.fastq.gz | Fastqsanger.gz | |||
| SRR3403081.fastq.gz | Fastqsanger.gz | |||
| SRR3403091.fastq.gz | Fastqsanger.gz |
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Project description:Identifying cellular mechanisms maintaining HIV-1 latency in the viral reservoir is crucial for devising effective cure strategies. Here we developed a flow cytometry-fluorescent in situ hybridization (flow-FISH) approach using a combination of probes that detects abortive and elongated HIV-1 transcripts for ex vivo isolation and characterization of viral reservoir cells in peripheral blood from people with HIV-1. Following the isolation of three distinct cell populations from CD4+ T cells (i.e. cells harboring transcriptionally latent HIV-1, cells harboring transcriptionally active HIV-1, or uninfected cells), we determined their transcriptomic profile by RNA sequencing (RNAseq). Supervised gene expression analysis identified several differentially expressed mitochondrial genes in infected cell populations compared to uninfected cells, but also in latently infected compared to productively infected CD4+ T cells. Our transcriptomic profiling data shows an association between diminished mitochondrial functioning and the transcriptional activity of the viral reservoir. These findings underline the relevance of metabolic regulation in HIV-1 infection, and support the development of strategies modulating immunometabolism to target viral latency.
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Project description:The epigenetic mechanisms established by histone modifications may affect the transcriptional silencing of HIV-1 and viral latency. A systematic epigenome profiling could be applicable to develop new epigenetic diagnostic markers for detecting HIV-1 latency. In this study, histone modification profiles of HIV-1 latency cell lines were compared with those of uninfected CD4+ T cell line. The HIV-1 latency gave rise to differential histone modification regions. The differential enrichment patterns helped us to define potential effector genes leading to the viral latency. The histone H3K4me3 and H3K9ac profiles were obtained from the HIV-1 latency cell lines (NCHA1, NCHA2, and ACH2) and control CD4+ T cell line (A3.01)
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Project description:To replicate in the host, HIV-1 must produce RNA and protein, and this depends cellular factors that also control gene expression. Recently, it has been shown that novel components of this machinery post-transcriptionally modify mRNAs with direct consequences for their structure and stability. The most common among these modifications is the addition of a methyl group to the N6 position of adenosine, termed m6A methylation. Here we are interested the interface of HIV-1 with this posttranscriptional mRNA modification pathway. We show that viral transcripts harbor a number of discrete methylation sites and are bound at those sites by these YTHDF proteins. These sites are conserved among distinct HIV-1 isolates and are observed during viral replication in numerous cell types. With reporter assays we also show that these sites stabilize mRNAs when compared to similar sequences mutated to be incapable of methylation. We further show that overexpression of these reader proteins boosts viral protein expression.
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Project description:The implementation of antiretroviral therapy (ART) has effectively restricted the transmission of Human Immunodeficiency Virus (HIV) and improved overall clinical outcomes. However, a complete cure for HIV remains out of reach, as the virus persists in a stable pool of infected cell reservoir that is resistant to therapy and thus a main barrier towards complete elimination of viral infection. While the mechanisms by which host proteins govern viral gene expression and latency are well-studied, the emerging regulatory functions of non-coding RNAs (ncRNA) in the context of T cell activation, HIV gene expression and viral latency have not yet been thoroughly explored. Here, we report the identification of the Cytoskeleton Regulator (CYTOR) long non-coding RNA (lncRNA) as an activator of HIV gene expression that is upregulated following T cell stimulation. Functional studies show that CYTOR suppresses viral latency by directly binding to the HIV promoter and associating with the cellular positive transcription elongation factor (P-TEFb) to activate viral gene expression. CYTOR also plays a global role in regulating cellular gene expression, including those involved in controlling actin dynamics. Depletion of CYTOR expression reduces cytoplasmic actin polymerization in response to T cell activation. In addition, treating HIV-infected cells with pharmacological inhibitors of actin polymerization reduces HIV gene expression. We conclude that both direct and indirect effects of CYTOR regulate HIV gene expression.
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Project description:The epigenetic mechanisms established by histone modifications may affect the transcriptional silencing of HIV-1 and viral latency. A systematic epigenome profiling could be applicable to develop new epigenetic diagnostic markers for detecting HIV-1 latency. In this study, histone modification profiles of HIV-1 latency cell lines were compared with those of uninfected CD4+ T cell line. The HIV-1 latency gave rise to differential histone modification regions. The differential enrichment patterns helped us to define potential effector genes leading to the viral latency.
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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.
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Project description:Distinct integration patterns of different retroviruses have puzzled virologists for over 20 years. The viral integrase (IN), as part of the intasome complex, docks onto the target DNA (tDNA) and catalyzes the insertion of the viral genome into the host chromatin. We identified retroviral IN amino acids directly contacting tDNA bases and affecting the local integration site sequence biases. These residues also determine the propensity of the virus to integrate into flexible tDNA sequences. Remarkably, natural polymorphisms INS119G and INR231G retarget viral integration away from gene dense regions, without affecting the interaction with the lentiviral tethering cofactor LEDGF/p75 (PSIP1). Precisely these variants were associated with rapid disease progression in a chronic HIV-1 subtype C infection cohort. These findings link integration site selection to virulence and viral evolution but also to the host immune response and antiretroviral therapy, since HIV-1 IN119 is under selection by HLA alleles and integrase inhibitors. LEDGF/p75 (PSIP1) ChIP-Seq using A300-848 antibody (recognizes p75 isoform) and input control in primary CD4+ T-cells
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