CIDR-NIDA Study of HIV Host Genetics
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ABSTRACT:
PROVIDER: PRJNA83629 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:CIDR: Genetics of Graft-vs-Host Disease
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Project description:CIDR: Genetics of Graft-vs-Host Disease
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Project description:CIDR: Collaborative Study on the Genetics of Alcoholism (COGA)
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Project description:<p>The overarching goal of this project is to identify and characterize genetic determinants of HIV 1 susceptibility and resistance in samples of African American (AA) and European American (EA) injection drug users (IDUs) by conducting (1) a case/control genome-wide association (GWA) study of HIV 1 infection (positive/negative); (2) a case-only GWA study of viral load among HIV+ IDUs. The study uses existing samples and data from Urban Health Study (UHS) (PI: Alex Kral), which was the longest-running study of street-recruited IDUs in North America, from 1986-2005. UHS was a serial, cross-sectional sero-epidemiological study. Data were collected every 6 months in communities with a high prevalence of injection drug use in the San Francisco Bay Area. It used targeted sampling in neighborhoods at easily accessible community field sites, such as churches, single room occupancy hotels, and community centers. Eligibility criteria for initial entry to the study were (1) injection drug use in past 30 days; (2) ability to provide informed consent; and (3) age 18 or older. The UHS cohort includes over 9,000 African American and European American IDUs whose serum samples have been stored and data are available on HIV antibody status, HIV risk behaviors, drug abuse and demographics.</p> <p>The current study includes 984 HIV+ cases and 2,243 HIV- controls. Approximately two HIV- controls per case were frequency matched on: (1) self-reported ancestry; (2) sex; (3) age; (4) year of ascertainment; and (5) HIV risk class. This GWAS (DA026141) was funded by the National Institute on Drug Abuse (NIDA; PI: Eric O. Johnson). Funding support for genotyping, which was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR), was provided by NIDA and the NIH contract "High throughput genotyping for studying the genetic contributions to human disease"(HHSN268200782096C). </p>
| phs000454.v1.p1 | EGA
Project description:<p>The overarching goal of this project is to identify and characterize genetic determinants of HIV 1 susceptibility and resistance in samples of African American (AA) and European American (EA) injection drug users (IDUs) by conducting (1) a case/control genome-wide association (GWA) study of HIV 1 infection (positive/negative); (2) a case-only GWA study of viral load among HIV+ IDUs. The study uses existing samples and data from Urban Health Study (UHS) (PI: Alex Kral), which was the longest-running study of street-recruited IDUs in North America, from 1986-2005. UHS was a serial, cross-sectional sero-epidemiological study. Data were collected every 6 months in communities with a high prevalence of injection drug use in the San Francisco Bay Area. It used targeted sampling in neighborhoods at easily accessible community field sites, such as churches, single room occupancy hotels, and community centers. Eligibility criteria for initial entry to the study were (1) injection drug use in past 30 days; (2) ability to provide informed consent; and (3) age 18 or older. The UHS cohort includes over 9,000 African American and European American IDUs whose serum samples have been stored and data are available on HIV antibody status, HIV risk behaviors, drug abuse and demographics.</p> <p>The current study includes 984 HIV+ cases and 2,243 HIV- controls. Approximately two HIV- controls per case were frequency matched on: (1) self-reported ancestry; (2) sex; (3) age; (4) year of ascertainment; and (5) HIV risk class. This GWAS (DA026141) was funded by the National Institute on Drug Abuse (NIDA; PI: Eric O. Johnson). Funding support for genotyping, which was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR), was provided by NIDA and the NIH contract "High throughput genotyping for studying the genetic contributions to human disease"(HHSN268200782096C). </p>
| phs000454 | dbGaP
Project description:HIV-1 persists as an integrated DNA provirus in infected cells. Antiretroviral therapy (ART) does not inhibit HIV-1 promoter activity. It is often assumed that HIV-1 reactivation versus latency passively follows host gene activation and repression near the HIV-1 integration site. HIV-1 proviruses integrated into active genes are then transcriptionally active, typically resulting in immune clearance of infected cells. HIV-1 proviruses integrated into repressive chromatin conversely escape immune surveillance. To understand how host gene activity affects HIV-1 transcription, we examined how CRISPR-mediated activation and inhibition of host genes affected HIV-1 nearby chromatin accessibility and RNA transcription using qPCR, ATAC-seq, and strand-specific RNA-seq, in seven Jurkat T cell clones having known HIV-1 integration site. We further examined host CRISPR-mediated HIV-1 activation and inhibition effects on host chromatin accessibility and RNA transcription. We found that host gene activation at the integration site decreased HIV-1 transcription, while host gene inhibition frequently increased HIV-1 transcription. Changes to transcription occurred in both HIV-1 orientations relative to the host gene. Particularly at same-orientation integration sites, reductions in HIV-1 transcription were accompanied by reduced chromatin accessibility at the HIV-1 promoter. However, when HIV-1 integrated in close proximity to host transcription start site, host gene activation increased HIV-1 transcription. When HIV-1 integrated into a non-genic region, we found that HIV-1 increased host chromatin accessibility, remained transcriptionally active, and drove high level of aberrant host RNA transcription. Overall, we found that instead of passively following host gene activity, HIV-1 shapes host chromatin accessibility while an interplay of host factors and transcriptional interference modulate its expression.
2025-10-21 | GSE302199 | GEO
Project description:HIV-1 persists as an integrated DNA provirus in infected cells. Antiretroviral therapy (ART) does not inhibit HIV-1 promoter activity. It is often assumed that HIV-1 reactivation versus latency passively follows host gene activation and repression near the HIV-1 integration site. HIV-1 proviruses integrated into active genes are then transcriptionally active, typically resulting in immune clearance of infected cells. HIV-1 proviruses integrated into repressive chromatin conversely escape immune surveillance. To understand how host gene activity affects HIV-1 transcription, we examined how CRISPR-mediated activation and inhibition of host genes affected HIV-1 nearby chromatin accessibility and RNA transcription using qPCR, ATAC-seq, and strand-specific RNA-seq, in seven Jurkat T cell clones having known HIV-1 integration site. We further examined host CRISPR-mediated HIV-1 activation and inhibition effects on host chromatin accessibility and RNA transcription. We found that host gene activation at the integration site decreased HIV-1 transcription, while host gene inhibition frequently increased HIV-1 transcription. Changes to transcription occurred in both HIV-1 orientations relative to the host gene. Particularly at same-orientation integration sites, reductions in HIV-1 transcription were accompanied by reduced chromatin accessibility at the HIV-1 promoter. However, when HIV-1 integrated in close proximity to host transcription start site, host gene activation increased HIV-1 transcription. When HIV-1 integrated into a non-genic region, we found that HIV-1 increased host chromatin accessibility, remained transcriptionally active, and drove high level of aberrant host RNA transcription. Overall, we found that instead of passively following host gene activity, HIV-1 shapes host chromatin accessibility while an interplay of host factors and transcriptional interference modulate its expression.
2025-10-21 | GSE302221 | GEO
Project description:Using HIV-1 RNASortSeq, 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 eight antiretroviral therapy treated, virally suppressed, HIV-1-infected individuals. Using custom bioinformatic pipeline, we identified HIV-1 genomic RNA, host RNA and HIV-1-host chimeric RNA junctions.
2021-04-01 | GSE112576 | GEO
Project description:Using microRNA array analyses of in vitro HIV-1-infected CD4+ cells, we find that several host microRNAs are significantly up- or downregulated around the time HIV-1 infection peaks in vitro. While microRNA-223 levels were significantly enriched in HIV-1-infected CD4+CD8? PBMCs, microRNA-29a/b, microRNA-155 and microRNA-21 levels were significantly reduced. Based on the potential for microRNA binding sites in a conserved sequence of the Nef-3?-LTR, several host microRNAs potentially could affect HIV-1 gene expression. Among those microRNAs, the microRNA-29 family has seed complementarity in the HIV-1 3?-UTR, but the potential suppressive effect of microRNA-29 on HIV-1 is severely blocked by the secondary structure of the target region. Our data support a possible regulatory circuit at the peak of HIV-1 replication which involves downregulation of microRNA-29, expression of Nef, the apoptosis of host CD4 cells and upregulation of microRNA-223. Time course of HIV infection on CD4 cells
2012-12-05 | E-GEOD-42737 | biostudies-arrayexpress