DOGMA-seq of opioid addiction treatment in HIV-1 infected individuals
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ABSTRACT:
PROVIDER: PRJNA981575 | ENA |
REPOSITORIES: ENA
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Project description:Opioid use and HIV-1 infection a impact immune function independently, but their impact on the immune system together is unknown. To understand the impact of opioids on immune function in HIV-1 infected individuals we used DOGMA-seq to examine the transcriptome, chromatin accessibility, and surface protein expression in HIV-1-infected individuals undergoing opioid addiction treatment.
2024-07-01 | GSE234521 | GEO
Project description:Due to the current opioid epidemic, a better understanding of genetic and environmental factors that contribute to opioid addiction is warranted. To explore the potential causative role of VitD in opioid addiction , we used multiple pharmacologic approaches and genetic mouse models. We used profiled the transcriptome of key brain reward regions upon morphine treatment in vitamin D receptor KO and wild type mice. Our results highlight the role of VitD deficiency in the development of addiction and suggest a potential therapeutic benefit of VitD supplementation for VitD deficient individuals in the prevention and management of addiction.
2021-04-25 | GSE171683 | GEO
Project description:Using HIV-1 SortSeq, we identified HIV-1-infected cells containing inducible HIV-1 for RNAseq from resting CD4+ T cells treated with PMA/ionomycin for 16 hours from HIV-1-infected, antiretroviral therapy treated, virally suppressed individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.
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Project description:Differentially expressed miRNAs between HIV-infected treatment-naïve individuals and HIV-negative individuals were found, and the altered signaling pathways were predicted using these differentially expressed miRNAs.
2016-01-15 | GSE76867 | GEO
Project description:Genome wide DNA Methylation in PBMC of untreated HIV-chronic individuals with different HIV control. For a total of 70 PBMC samples we determined DNA Methylation levels of more than 450,000 CpG sites with the platform Infinium HumanMethylation450 BeadChip (450K, Illumina). Finally, we compared DNA methylation between HIV-High (>50,000 HIV RNA copies/ml, n=29) and HIV-Low (<10,000 HIV RNA copies/ml, n=41) individuals and identified 2,649 gene-annotated CpG positions that were differentially methylated between the two groups.
2020-07-02 | GSE140800 | GEO
Project description:HIV-1 SortSeq identifies HIV-1-infected cells from HIV-1-infected individuals
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Project description:Recently, several neutralizing anti-HIV antibodies have been isolated from memory B cells of HIV-infected individuals. However, despite extensive evidence of B-cell dysfunction in HIV disease, little is known about the cells from which these rare HIV-specific antibodies originate. Accordingly, HIV envelope gp140 and CD4 or co-receptor (CoR) binding site (bs) mutant probes were used to evaluate HIV-specific responses in the peripheral blood B cells of individuals at various stages of infection. In contrast to non-HIV responses, HIV-specific responses against gp140 were enriched within abnormal B cells, namely activated and exhausted memory subsets, which are largely absent in the blood of uninfected individuals. Responses against the CoRbs (a poorly-neutralizing epitope) arose early whereas those against the CD4bs (a well-characterized neutralizing epitope) were delayed and infrequent. Enrichment of the HIV-specific response within resting memory B cells, the predominant subset in uninfected individuals, did occur in certain infected individuals who maintained low levels of plasma viremia and immune activation with or without antiretroviral therapy. These findings were corroborated by transcriptional profiles. Taken together, our findings provide valuable insight into virus-specific B-cell responses in HIV infection and demonstrate that memory B-cell abnormalities may contribute to the ineffectiveness of the antibody response in infected individuals.
2014-06-24 | GSE56499 | GEO
Project description:Vitamin D deficiency exacerbates UV/endorphin and opioid addiction
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Project description:Recently, several neutralizing anti-HIV antibodies have been isolated from memory B cells of HIV-infected individuals. However, despite extensive evidence of B-cell dysfunction in HIV disease, little is known about the cells from which these rare HIV-specific antibodies originate. Accordingly, HIV envelope gp140 and CD4 or co-receptor (CoR) binding site (bs) mutant probes were used to evaluate HIV-specific responses in the peripheral blood B cells of individuals at various stages of infection. In contrast to non-HIV responses, HIV-specific responses against gp140 were enriched within abnormal B cells, namely activated and exhausted memory subsets, which are largely absent in the blood of uninfected individuals. Responses against the CoRbs (a poorly-neutralizing epitope) arose early whereas those against the CD4bs (a well-characterized neutralizing epitope) were delayed and infrequent. Enrichment of the HIV-specific response within resting memory B cells, the predominant subset in uninfected individuals, did occur in certain infected individuals who maintained low levels of plasma viremia and immune activation with or without antiretroviral therapy. These findings were corroborated by transcriptional profiles. Taken together, our findings provide valuable insight into virus-specific B-cell responses in HIV infection and demonstrate that memory B-cell abnormalities may contribute to the ineffectiveness of the antibody response in infected individuals. HIV-specific responses against gp140 were enriched within abnormal B cells, namely activated (AM) and exhausted (tissue-like; TLM) memory subsets, which are largely absent in the blood of uninfected individuals. These responses are highest during the early stage of HIV infection, significantly decreased following the initiation of antiretroviral therapy (ART), and most importantly, enriched in normal resting memory B cells (RM) when HIV viremia and immune activation are controlled either naturally or as a result of ART. These HIV-specific B cells (AM and TLM) and resting memory B cells (RM) were sorted from peripheral blood mononuclear cells (PBMCs) of 6 HIV infected individuals. In addition, gp140-specific IgG+ B cells were sorted from individuals with either a strong (n= 6) or weak (n= 6) pro-resting memory profile. TaqMan gene expression assay was performed on these HIV-specific B cells and B cell subset. The array consisted of 29 genes.
2014-06-24 | E-GEOD-56499 | biostudies-arrayexpress
Project description:The illicit use of synthetic opioids such as fentanyl has led to a serious public health crisis in the United States. People with opioid use disorder are more likely to contract infections such as HIV and viral hepatitis. While several drugs of abuse are known to enhance viral replication and to suppress immunologic responses, the effects of synthetic opioids on HIV pathogenesis have not been investigated thoroughly. Thus, we examined the impact of fentanyl on HIV-susceptible and HIV-infected cell types and chemokine receptor expression in vitro. TZM-bl and HIV-infected lymphocyte cells were incubated with fentanyl at concentrations of 1 ng, 100 ng, and 10 ug. Expression levels of the CXCR4 and CCR5 chemokine receptors were measured in cell lysates, and HIV p24 antigen was quantified in culture supernatants by ELISA. HIV proviral DNA was quantified in cells using SYBR RT-PCR targeting the pol gene. Cell viability in the presence of drug was detected by the MTT Cell Proliferation Assay. RNA-seq and miRNAseq was performed to characterize cellular gene regulation in the presence of fentanyl. Fentanyl enhanced expression of CXCR4 and CCR5 protein levels in a dose-dependent manner in HIV-susceptible and HIV-infected cells. Similarly, fentanyl induced viral expression in HIV-exposed TZM-bl cells and in multiple HIV-infected lymphocyte cell lines. Multiple genes associated with apoptosis, antiviral / interferon response, chemokine signaling, and NFκB signaling were differentially regulated by fentanyl. These data demonstrate that the synthetic opioid fentanyl impacts HIV replication and chemokine co-receptor expression in HIV-susceptible and HIV-infected cells. Increased virus levels also suggest that opioid use may increase the likelihood of transmission to others and accelerate disease progression.
2022-10-19 | GSE216044 | GEO