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Transcriptomic analysis reveals key pathways influenced by HIV-2 Vpx

ABSTRACT: Transcriptomic analysis reveals key pathways influenced by HIV-2 Vpx

PROVIDER: PRJNA979175 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24819889.fastq.gz	Fastqsanger.gz
	SRR24819890.fastq.gz	Fastqsanger.gz
	SRR24819891.fastq.gz	Fastqsanger.gz
	SRR24819892.fastq.gz	Fastqsanger.gz
	SRR24819893.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis reveals key pathways influenced by HIV-2 Vpx

Project description:Viral protein X (Vpx) is a unique accessory protein encoded by the genome of the Human immunodeficiency virus type 2 (HIV-2) and lineages of the simian immunodeficiency virus of sooty mangabeys. So far, counteracting the cellular restriction factor SAMHD1 and mediating efficient translocation of viral pre-integration complex have been recognized as key functions of Vpx, however, thorough exploration of its effects on the cellular transcriptome and cytokine milieu have not yet been explored. In this study, we carried out transcriptomic analysis of THP-1 cells and determined differential gene expression induced by HIV-2 Vpx, additionally, we measured the effect of Vpx expression on secretion of key cytokines in the medium of transfected cells. Our findings revealed that wild-type HIV-2 Vpx can significantly alter the expression of genes coding for helicases, zinc finger proteins, chaperons, transcription factors and proteins involved in DNA methylation. Differentially altered genes were involved in negative regulation of viral process; type I interferon signaling pathway; DNA-templated transcription, elongation; positive regulation of interferon-beta production and negative regulation of innate immune response. Moreover, Vpx downregulated genes associated with negative regulation of TGF-β1, resulting in stimulation of its production. Importantly, Vpx was also found to decrease the expression of HIV-2 Tat, possibly through downregulation of a crucial splicing factor required for maturation of Tat.

2025-04-30 | GSE233999 | GEO

Drug screen combining RNA landscape analysis reveals targetable pathways in HIV-1 reactivation

Project description:We invesitgated cellular pathways required for HIV-1 activation using HIV-1-suppressing agents. Despite effective antiretroviral therapy, HIV-1-nfected cells continue to produce viral antigens and induce chronic immune exhaustion. Using a novel dual reporter system and a high-throughput drug screen, we identified FDA-approved drugs which can suppress HIV-1 reactivation in both cell line models and CD4+ T cells from virally suppressed, HIV-1-infected individuals. We identified 11 cellular pathways required for HIV-1 reactivation as druggable targets. Using differential expression analysis, gene set enrichment analysis and exon-intron landscape analysis, we examined the impact of drug treatment on the cellular environment at a genome-wide level.

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Altered pattern of circulating miRNAs in HIV lipodystrophy perturbs key adipose differentiation and inflammation pathways

Project description:Altered pattern of circulating miRNAs in HIV lipodystrophy perturbs key adipose differentiation and inflammation pathways

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The translational landscape of HIV-1 infected cells reveals key gene regulatory principles

Project description:Human immunodeficiency virus-1 (HIV-1) uses a number of strategies to modulate viral and host gene expression during its life cycle. To characterize the transcriptional and translational landscape of HIV-1 infected cells, we used a combination of ribosome profiling, disome sequencing and RNA sequencing. We show that HIV-1 messenger RNAs are efficiently translated at all stages of infection, despite evidence for a substantial decrease in the translational efficiency of host genes that are implicated in host cell translation. Our data identify upstream open reading frames in the HIV-1 5′-untranslated region as well as internal open reading frames in the Vif and Pol coding domains. We also observed ribosomal collisions in Gag-Pol upstream of the ribosome frameshift site that we attributed to an RNA structural fold using RNA structural probing and functional analysis. Antisense oligonucleotides designed to alter the base of this structure decreased frameshift efficiency. Overall, our data highlight the complexity of HIV-1 gene regulation and provide a key resource for decoding of host–pathogen interactions upon HIV-1 infection. Furthermore, we provide evidence for a RNA structural fold including the frameshift site that could serve as a target for antiviral therapy.

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Molecular Pathways are influenced by Progranulin in a neuronal cell model

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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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