Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22560300_1.fastq.gz | Fastqsanger.gz | |||
| SRR22560300_2.fastq.gz | Fastqsanger.gz | |||
| SRR22560301_1.fastq.gz | Fastqsanger.gz | |||
| SRR22560301_2.fastq.gz | Fastqsanger.gz | |||
| SRR22560302_1.fastq.gz | Fastqsanger.gz |
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Project description:Context: Although androgen treatment increases muscle mass in HIV-infected men, the underlying mechanisms are poorly understood. Analysis of genome-wide microarray data obtained from skeletal muscle biopsies can be used to profile androgen-regulated pathways. Objective: To identify genes and pathways associated with testosterone treatment and myogenesis in the context of HIV-infected men using genome-wide microarray analysis of skeletal muscle biopsies. Results: A significant weight gain was observed in subjects treated with testosterone compared to placebo (+2.05 kgs and –1.07 kgs, respectively; P = 0.003) as well as gains in DEXA lean mass (2.93 kgs vs. 0.35 kgs, respectively; P = 0.003). Microarray expression profiles and RTPCR validation of RNA after 14 days of treatment indicated that several gene sets including transcriptional control, myogenesis, adipogenesis, insulin signaling, apoptosis, cell cycle, chromatin remodeling, and stress response genes were differentially expressed with testosterone treatment. Protein expression analysis of myogenic differentiation and protein synthesis markers (MyoD, Myogenin, phosphorylated p38 MAPK and phosphorylated AKT) in muscle biopsies and skeletal muscle cells treated with DHT confirmed that testosterone engages a network of pro-myogenic genes. Conclusions: Testosterone-associated gain in muscle mass in HIV-infected men engaged a network of regulatory pathways involved in broad transcriptional control, myogenesis, insulin signaling, chromatin remodeling, and stress response. Further evaluation of precise signaling intermediates within androgen regulated pathways may help to better define improvements in muscle mass, both in healthy and HIV infected patients. Keywords: Dose Response, Myogenesis
2007-08-29 | GSE5106 | GEO
Project description:The continuing spread of HIV/AIDS is predominantly fueled by sexual exposure to HIV-contaminated semen. Seminal plasma (SP), the liquid portion of semen, harbors a variety of factors that may favor HIV transmission by facilitating viral entry into host cells, eliciting the production of pro-inflammatory cytokines, and enhancing the translocation of HIV across the genital epithelium. One important and abundant class of factors in SP is extracellular vesicles (EVs), which in general are important intercellular signal transducers. Although numerous studies have characterized blood plasma-derived EVs from both uninfected and HIV-infected individuals, little is known about the properties of EVs from semen of HIV-infected individuals. We report here that fractionated SP enriched for EVs from HIV-infected men induce potent transcriptional responses in epithelial and stromal cells that interface with luminal contents of the female reproductive tract. Compared to semen EV fractions from uninfected individuals, those from acutely-infected individuals induced a more pro-inflammatory signature. This was not associated with any observable differences in the surface phenotypes of the vesicles. However, miRNA expression profiling analysis revealed that EV fractions from infected individuals exhibit a broader and more diverse profile. Taken together, our data suggest that SP EVs from HIV-infected individuals exhibit unique miRNA signatures and exert potent pro-inflammatory transcriptional changes in cells of the female reproductive tract, which may facilitate HIV transmission.
2020-06-18 | GSE152714 | GEO
Project description:Context: Although androgen treatment increases muscle mass in HIV-infected men, the underlying mechanisms are poorly understood. Analysis of genome-wide microarray data obtained from skeletal muscle biopsies can be used to profile androgen-regulated pathways. Objective: To identify genes and pathways associated with testosterone treatment and myogenesis in the context of HIV-infected men using genome-wide microarray analysis of skeletal muscle biopsies. Results: A significant weight gain was observed in subjects treated with testosterone compared to placebo (+2.05 kgs and â??1.07 kgs, respectively; P = 0.003) as well as gains in DEXA lean; mass (2.93 kgs vs. 0.35 kgs, respectively; P = 0.003). Microarray expression profiles and RTPCR validation of RNA after 14 days of treatment indicated that several gene sets including; transcriptional control, myogenesis, adipogenesis, insulin signaling, apoptosis, cell cycle, chromatin remodeling, and stress response genes were differentially expressed with testosterone treatment. Protein expression analysis of myogenic differentiation and protein synthesis markers (MyoD, Myogenin, phosphorylated p38 MAPK and phosphorylated AKT) in muscle biopsies and skeletal muscle cells treated with DHT confirmed that testosterone engages; a network of pro-myogenic genes. Conclusions: Testosterone-associated gain in muscle mass in HIV-infected men engaged a network of regulatory pathways involved in broad transcriptional control, myogenesis, insulin signaling, chromatin remodeling, and stress response. Further evaluation of precise signaling intermediates within androgen regulated pathways may help to better define improvements in muscle mass, both in healthy and HIV infected patients. Experiment Overall Design: Design, Setting, and Participants: 44 HIV+ men with weight loss were randomized to receive either 300mg testosterone enanthate or placebo injections IM weekly for 16 weeks. Muscle Experiment Overall Design: biopsies were obtained at baseline and on treatment day 14. A random subset of specimens was chosen for microarray analysis; changes in selected genes were confirmed by reverse transcriptase - polymerase chain reaction (RT-PCR), and western blot analysis. Human skeletal Experiment Overall Design: myogenic precursor cells (SkMCs) were cultured in vitro in the presence of dihydrotestosterone (DHT) to evaluate activation of myogenic protein expression. Experiment Overall Design: Main outcome measures: Relative RNA levels in skeletal muscle biopsies were measured by expression profiling with microarrays and expression levels were validated in samples using quantitative RT-PCR. Further confirmation of changes in key myogenic biomarkers was obtained in DHT treated SkMCs.
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2017-12-01 | GSE103555 | 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:Cellular composition and responsiveness of immune system evolve upon ageing and are influenced by biological sex. CD4+ T cells from women living with HIV exhibit decreased viral replication ex vivo compared to men. We thus hypothesized that these findings could be recapitulated in vitro, and infected primary CD4+ T cells with HIV-based vectors pseudotyped with VSV-G or HIV envelopes. We used cells isolated from twenty donors to interrogate the effect of sex and age on permissiveness over a six-day activation kinetics. Our data identified an increased permissiveness to HIV between 24 and 72h post-stimulation. Sex- and age-based analysis at these time points showed increased susceptibility to HIV of cells isolated from males and from donors over 50 years old, respectively. Parallel assessment of surface marker expression revealed higher frequencies of activation markers (CD69, CD25, HLA-DR) and immune check point inhibitors (PD-1 and CTLA-4 in cells from highly permissive donors. Furthermore, positive correlations were identified between CD69, PD-1 and CTLA-4 expression kinetics and HIV expression kinetics. Cell population heterogeneity was assessed by single-cell RNA-Seq analysis and no cell subtype enrichment was identified according to sex. Finally, transcriptomic analyses further highlighted the role of activation in those differences with enriched activation and cell cycle gene sets in men and in older women cells. Altogether, this study brought further evidence about individual features affecting HIV replication at the cellular level and should be considered in latency reactivation studies for HIV cure.
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Project description:Cellular composition and responsiveness of immune system evolve upon ageing and are influenced by biological sex. CD4+ T cells from women living with HIV exhibit decreased viral replication ex vivo compared to men. We thus hypothesized that these findings could be recapitulated in vitro, and infected primary CD4+ T cells with HIV-based vectors pseudotyped with VSV-G or HIV envelopes. We used cells isolated from twenty donors to interrogate the effect of sex and age on permissiveness over a six-day activation kinetics. Our data identified an increased permissiveness to HIV between 24 and 72h post-stimulation. Sex- and age-based analysis at these time points showed increased susceptibility to HIV of cells isolated from males and from donors over 50 years old, respectively. Parallel assessment of surface marker expression revealed higher frequencies of activation markers (CD69, CD25, HLA-DR) and immune check point inhibitors (PD-1 and CTLA-4 in cells from highly permissive donors. Furthermore, positive correlations were identified between CD69, PD-1 and CTLA-4 expression kinetics and HIV expression kinetics. Cell population heterogeneity was assessed by single-cell RNA-Seq analysis and no cell subtype enrichment was identified according to sex. Finally, transcriptomic analyses further highlighted the role of activation in those differences with enriched activation and cell cycle gene sets in men and in older women cells. Altogether, this study brought further evidence about individual features affecting HIV replication at the cellular level and should be considered in latency reactivation studies for HIV cure.
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Project description:There is scant data on the mechanisms through which asymptomatic STIs (aSTIs) alter risk of HIV acquisition in the male genital tract. Foreskin removal lowers the risk of HIV acquisition, but molecular events leading to this protection are unclear. Here we show that an asymptomatic urethral infection with Chlamydia trachomatis significantly alters the foreskin epithelial proteome composition. We developed and optimised a shotgun liquid chromatography coupled tandem mass spectrometry based proteomics approach and applied this to foreskins collected at the time of medical male circumcision from 16 aSTI+ cis-gender men and 10 age-matched STI- controls. We used a novel bioinformatic metaproteomic pipeline to detect differentially expressed proteins. Gene enrichment ontology analysis revealed proteins associated with inflammatory and immune activation function in both inner and outer foreskin from men with an aSTI. Neutrophil activation/degranulation and viral-evasion proteins were significantly enriched in foreskins from men with aSTI whereas homotypic cell-cell adhesion proteins were enriched in foreskin tissue from men without an STI. Collectively, our data show that an asymptomatic urethral sexually transmitted infection result in profound alterations in epitheial tissue that potentially causes depletion of barrier integrity and function and that may encourage HIV susceptibilty.
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