Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7724040.fastq.gz | Fastqsanger.gz | |||
| SRR7724040_1.fastq.gz | Fastqsanger.gz | |||
| SRR7724040_2.fastq.gz | Fastqsanger.gz | |||
| SRR7724050_1.fastq.gz | Fastqsanger.gz | |||
| SRR7724050_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:We used the technology of MNase-seq and capture-based target enrichment to analyze nucleosome positioning on the HIV DNA.
2020-03-02 | GSE135551 | GEO
Project description:We used the technology of MNase-seq and capture-based target enrichment to analyze nucleosome positioning on the HIV DNA.
2020-03-02 | GSE139556 | GEO
Project description:MiRNAs and other small noncoding RNAs (sncRNAs) are key players in post-transcriptional gene regulation. HIV-1 derived small noncoding RNAs (sncRNAs) have been described in HIV-1 infected cells, but their biological functions still remain to be elucidated. Here, we approached the question whether viral sncRNAs may play a role in the RNA interference (RNAi) pathway or whether viral mRNAs are targeted by cellular miRNAs in human monocyte-derived macrophages (MDM). The incorporation of viral sncRNAs and/or their target RNAs into RNA-induced silencing complex was investigated using photoactivatable ribonucleoside-induced cross-linking and immunoprecipitation (PAR-CLIP) as well as high-throughput sequencing of RNA isolated by cross-linking immunoprecipitation (HITS-CLIP), which capture Argonaute2-bound miRNAs and their target RNAs. HIV-1 infected monocyte-derived macrophages (MDM) were chosen as target cells, as they have previously been shown to express HIV-1 sncRNAs. In addition, we applied small RNA deep sequencing to study differential cellular miRNA expression in HIV-1 infected versus non-infected MDMs. PAR-CLIP and HITS-CLIP data demonstrated the absence of HIV-1 RNAs in Ago2-RISC, although the presence of a multitude of HIV-1 sncRNAs in HIV-1 infected MDMs was confirmed by small RNA sequencing. Small RNA sequencing revealed that 1.4% of all sncRNAs were of HIV-1 origin. However, neither HIV-1 derived sncRNAs nor putative HIV-1 target sequences incorporated into Ago2-RISC were identified, suggesting that HIV-1 sncRNAs are not involved in the canonical RNAi pathway nor is HIV-1 targeted by this pathway in HIV-1 infected macrophages.
2015-07-14 | GSE70851 | GEO
Project description:Macrophages are a major target for human immunodeficiency virus type 1 (HIV-1) infection. However, macrophages are largely heterogeneous and may exhibit differences in permissiveness to HIV-1 infection. This study highlights the interplay of macrophage heterogeneity in HIV-1 pathogenesis. We show that monocyte-derived macrophages (MDM) could be divided into two distinct subsets: CD14+Siglec-1hiCD4+ (non-adherent MDM), and CD14+Siglec-1LoCD4- (adherent MDM). The CD14+Siglec-1hiCD4+MDM subset represented the smaller proportion in the macrophage pool, and varied among different donors. Fractionation and subsequent exposure of the two MDM subsets to HIV-1 revealed opposite outcomes in terms of HIV-1 capture and infection. Although the CD14+Siglec-1hiCD4+MDM captured significantly more HIV-1, infection was significantly higher in the CD14+Siglec-1LoCD4-MDM subset. Thus, CD14+Siglec-1hiCD4+MDM were less permissive to infection. Depletion of CD14+Siglec-1hiCD4+MDM or a decrease in their percentage, resulted in increased infection of MDM, suggestive of a capacity of these cells to capture and sequester HIV-1 in an environment that hinders its infectivity. Increased expression of innate restriction factors and cytokine genes were observed in the non-adherent CD14+Siglec-1hiCD4+MDM, both before and after HIV-1 infection, compared to the adherent CD14+Siglec-1LoCD4-MDM. The differential expression of gene expression profiles in the two macrophage subsets may provide an explanation for the differences observed in HIV-1 infectivity.
2018-02-22 | GSE103666 | GEO
Project description:The heterogeneity and rarity of HIV-1-infected cells hampers effective cure strategies. We used single-cell DOGMA-seq to simultaneously capture transcription factor accessibility, transcriptome, 156 surface proteins, HIV-1 DNA, and HIV-1 RNA from six HIV-1+ individuals during viremia and after suppressive antiretroviral therapy. We identified 252 transcriptionally inactive (HIV-1 DNA+ RNA–) and 270 transcriptionally active (HIV-1 RNA+) HIV-1-infected cells from 82,549 memory CD4+ T cells. We identified increased transcription factor accessibility in HIV-1 DNA+ RNA– cells (RORC) and HIV-1 RNA+ cells (IRF and AP-1), in addition to CNC and MAF in both. Both HIV-1 DNA+ RNA– and HIV-1 RNA+ cells upregulate IKZF3 (Aiolos) that correlates with proliferation of HIV-1-infected cells. We revealed that the heterogeneous HIV-1-infected T cells comprise four distinct immune programs driven by epigenetic regulators – IRF-activation, Eomes-cytotoxic effector, AP-1-migration, and cell death. Our study revealed the single-cell epigenetic, transcriptional, and protein states of transcriptionally inactive and active HIV-1-infected cells.
2023-09-20 | GSE239915 | GEO
Project description:Background: The cellular reservoir of latent HIV infection remains the main barrier to cure this virus. Elimination of this reservoir would be possible, if molecular identity of latently infected cells were fully elucidated. Biomarkers proposed previously were able to capture only a relatively small fraction of all reservoir cells. In the present study, we set out to conduct comprehensive molecular profiling, at the protein and RNA levels, of CD4+ T cells latently infected with HIV in vitro, using liquid chromatography-mass spectrometry (LC-MS) and RNA sequencing (RNA-Seq), respectively. Protein-based methods such as quantitative proteomic profiling using LC-MS may be more beneficial due to direct transferability of results to antibody-based approaches to capture latently infected cells. Integrated analysis of proteomic and transcriptomic data adds a level of validation and increases confidence in identified biomarkers. Flow cytometry and integrated HIV DNA assay were further used to enrich for latently infected cells with antibodies against selected biomarker proteins. Results: Using quantitative proteomics, we identified a total of 10,886 proteins (peptide level FDR < 0.05), of which 673 were up- and 780 down-regulated in latently infected compared to mock-infected cells in vitro (p < 0.05). Among these proteins, 21 were dysregulated at the RNA level in the same direction. Pathway analysis identified p53, mTOR, Wnt and NOTCH signaling, demonstrating that our in vitro model reflects known mechanisms of latency establishment and maintenance. Comparison of identified proteins with other proteomics studies revealed that identified molecular signatures of latency depend on technology and cell types used; however, a subset of proteins were identified both in the present, and at least one other study. Antibodies against selected protein markers, CEACAM1 and PLXNB2, could enrich for latently infected cells from mixed cell population 3-10 fold (5.8 fold average, p < 0.001). Conclusion: Two new molecules, CEACAM1 and PLXNB2, were identified as biomarkers for HIV latency. However, the level of enrichment for latently infected cells compared to biomarkers proposed previously was not improved. These results are consistent with the idea that each proposed biomarker defines only a subset of latently infected cells, and that a combined biomarker will be required to capture or target the latent HIV reservoir represented by different cell types.
2023-10-24 | PXD024014 | Pride
Project description:RattanID - target capture
| PRJEB61468 | ENA