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ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

ABSTRACT: ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease. Blood samples were taken from 20 individuals at week 0 (before treatement) and week 12. 10 individuals received chloroquine 250mg orally and 10 individuals received placebo.

ORGANISM(S): Homo sapiens

SUBMITTER: Gregory Tharp

PROVIDER: E-GEOD-71064 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

Project description:ACTG A5258, we asked whether chloroquine could reduce the immune activation in HIV infection posited to be driven by microbial TLR agonists, such as bacterial elements translocated from the gut and HIV-1 RNAs . We anticipate that blocking this activation pathway might interfere with events in pathogenesis leading to AIDS- and non-AIDS-related clinical manifestations of HIV disease. Blood samples were taken from 20 individuals at week 0 (before treatement) and week 12. 10 individuals received chloroquine 250mg orally and 10 individuals received placebo.

2016-07-15 | E-GEOD-71063 | biostudies-arrayexpress

ACTG A5258 Clinical administration of chloroquine to HIV-infected patients receiving antiretroviral therapy to reduce immune activation

2016-07-15 | GSE71064 | GEO

ACTG A5258 Clinical administration of chloroquine to patients with untreated chronic HIV infection to reduce immune activation

2016-07-15 | GSE71063 | GEO

Epigenetic Features of HIV-Induced T-Cell Exhaustion Persist Despite Early Antiretroviral Therapy

Project description:T cell dysfunction occurs early following HIV infection, impacting the emergence of non-AIDS morbidities and limiting curative efforts. ART initiated during primary HIV infection (PHI) can reverse this dysfunction, but the extent of recovery is unknown. We studied 66 HIV-infected individuals treated from early PHI with up to three years of ART. Compared with HIV-uninfected controls, CD4 and CD8 T cells from early HIV infection were characterised by T cell activation and increased expression of the immune checkpoint receptors (ICRs) PD1, Tim-3 and TIGIT. Three years of ART lead to partial – but not complete – normalisation of ICR expression, the dynamics of which varied for individual ICRs. For HIV-specific cells, epigenetic profiling of tetramer-sorted CD8 T cells revealed that epigenetic features of exhaustion typically seen in chronic HIV infection were already present early in PHI, and that ART initiation during PHI resulted in only a partial shift of the epigenome to one with more favourable memory characteristics. These findings suggest that although ART initiation during PHI results in significant immune reconstitution, there may be only partial resolution of HIV-related phenotypic and epigenetic changes.

2023-07-19 | GSE237729 | GEO

Clinical administration of chloroquine to HIV-infected patients that are untreated or receiving antiretroviral therapy

Project description:Clinical administration of chloroquine to HIV-infected patients that are untreated or receiving antiretroviral therapy

| PRJNA290205 | ENA

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

Project description:Anti-malaria drug chloroquine has been used as an anti-inflammatory agent for treating systemic lupus erythematosus and rheumatoid arthritis, without clear mechanism of action. Here we report that chloroquine potently inhibits the expression of proinflammatory cytokines through transrepression of glucocorticoid receptor (GR). Instead of direct binding to GR, chloroquine synergistically activates glucocorticoid signaling via inhibition of lysosomal functions. In mouse collagen induced arthritis model, chloroquine synergizes the therapeutic effects of glucocorticoid. Lysosomal inhibition by bafilomycin A1, an inhibitor of V-type ATPase, or by knockdown of transcription factor EB (TFEB), a master activator of lysosomal biogenesis, mimics the effects of chloroquine. These results reveal an unexpected regulation of glucocorticoid signaling by lysosomes and provide a mechanistic basis for treating inflammation and autoimmune diseases by combination of glucocorticoids and lysosomal inhibitors.

2012-01-18 | GSE24579 | GEO

Potentiation of glucocorticoid signaling by chloroquine via inhibition of lysosomes

2012-01-18 | E-GEOD-24579 | biostudies-arrayexpress

Effect of HIV infection and antiretroviral therapy initiation on genome-wide DNA methylation patterns.

Project description:Background. Previous epigenome-wide association studies have shown that HIV infection can disrupt the host DNA methylation landscape. However, it remains unclear how antiretroviral therapy (ART) affects the HIV-induced epigenetic modifications. Methods. 184 individuals with HIV from the NEAT001/ANRS143 clinical trial (with pre-ART and post-ART samples [96 weeks of follow-up]) and 44 age-and-sex matched individuals without HIV were included. We compared genome-wide DNA methylation profiles in whole blood between groups adjusting for age, sex, batch effects, and leucocyte type heterogeneity. Findings. We identified 430 differentially methylated positions (DMPs) between HIV+ pre-ART individuals and HIV-uninfected controls. In participants with HIV, ART initiation modified the DNA methylation levels at 845 CpG positions and restored 49.3% of the changes found between HIV+ pre-ART and HIV-uninfected individuals. We only found 15 DMPs when comparing DNA methylation profiles between HIV+ post-ART individuals and participants without HIV. The Gene Ontology enrichment analysis of DMPs associated with untreated HIV infection revealed an enrichment in biological processes regulating the immune system and antiviral responses. In participants with untreated HIV infection, DNA methylation levels at top HIV-related DMPs were associated with CD4/CD8 ratios and viral loads. Changes in DNA methylation levels after ART initiation were weakly correlated with changes in CD4+ cell counts and the CD4/CD8 ratio. Interpretation. Control of HIV viraemia after 96 weeks of ART initiation restores most of the host DNA methylation changes that occurred before antiretroviral treatment of HIV infection.

2023-01-16 | GSE217633 | GEO

Metabolite variation in the blood serum of HIV carrier patients treated with effervescent glutamine

Project description:It was demonstrated that effervescent glutamine supplementation in people living with HIV/AIDS increased the amount of CD4+ T lymphocytes. , decreased the serum levels of biomarkers of inflammation, and introduced health benefits. Herein, NMR spectroscopy was applied to evaluate if oral ingestion of glutamine (12.5 g) for 30 days can be measured through serum metabolite variations and if the reported benefits might correlate to small metabolites' changes in a chosen cohort of individuals. The HIV/AIDS group has been carefully selected and studied before and after the 30-days of supplementation with the glutamine, together with the matched non-HIV carrier patients' group. The group of HIV/AIDS individuals presented lower (p < 0.05) levels of choline, creatine, pyruvate, glutamate, lysine, and tyrosine when compared to the non-HIV carrier patients. On the other hand, serum concentrations of glucose, lipids, lactate, glutamine, phenylalanine, and threonine were higher (p < 0.05) in HIV/AIDS individuals. The variation in metabolites as a result of treatment with glutamine is consistent with the improvements observed in these patients and may lead us to suggest the introduction of the effervescent glutamine supplementation to antiretroviral therapies in people living with HIV/AIDS.

2022-03-31 | ST002133 | MetabolomicsWorkbench

Transcriptomic analysis to identify genes associated with chloroquine-mediated radiosensitization of glioblastoma stem cells

Project description:Tumour suppressor p53 regulates hundreds of genes by either activating or repressing their transcription. p53-dependent transcription is activated by stress factors such as DNA damage, reactive oxygen species, hypoxia or oncogenic signaling. Lysosomotropic agent and DNA intercalating agent chloroquine has been implicated in sensitizing glioblastoma to radiation via p53 pathway. This study evaluates the effects of chloroquine in glioblastoma stem cells differing for the status of TP53 by using an integrated approach encompassing in vitro, in vivo and in silico methodologies to characterize the impacts of chloroquine on cell vitality, tumor-propagating capacity and gene expression. We used microarrays to identify the genes whose expression is influenced by DNA intercalator chloroquine (ClQ) in glioblastoma stem cells expressing wild type p53 (line #993), mutant p53 (line G112) or a p53 null line #1095. To compare chloroquine-associated transcriptomic changes with those induced by ionizing radiation (IR), samples of IR-treated line #993 ("#993_IR") were analyzed in parallel with ClQ-treated samples ("993_ClQ").

2023-08-04 | GSE225191 | GEO

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