Similar Datasets
Project description:Analysis of RISC bound short (s)RNAs in cells infected with HIV-1 reveals a contribution of 6mer seed toxicity to HIV-1 induced cytopathicity
2023-06-07 | GSE218193 | GEO
Project description:Analysis of RISC bound short (s)RNAs in cells infected with HIV-1 reveals a contribution of 6mer seed toxicity to HIV-1 induced cytopathicity
2023-06-07 | GSE218187 | GEO
Project description:Analysis of RISC bound short (s)RNAs in cells infected with HIV-1 reveals a contribution of 6mer seed toxicity to HIV-1 induced cytopathicity
2023-06-07 | GSE218192 | GEO
Project description:Analysis of RISC bound short (s)RNAs in cells infected with HIV-1 reveals a contribution of 6mer seed toxicity to HIV-1 induced cytopathicity
2023-06-07 | GSE218191 | GEO
Project description:Analysis of RISC bound short (s)RNAs in cells infected with HIV-1 reveals a contribution of 6mer seed toxicity to HIV-1 induced cytopathicity
2023-06-07 | GSE218189 | GEO
Project description:Introduction of antiretroviral therapy has limited the spread of HIV and improved clinical outcomes. Yet, a complete cure for infection remains out of reach, as in the face of therapy, a transcriptionally silent but replication-competent provirus persists in a long-lived cell reservoir. Towards identifying new host proteins that regulate HIV gene transcription and latency, we performed a genome-wide CRISPR knockout screen in human CD4+ T cells. We identified the Activating Transcription Factor as a regulator of HIV gene transcription. ATF1 is recruited to the HIV promoter and activates viral gene expression. Gain and loss of function experiments demonstrate that depletion of ATF1 expression decreases HIV gene expression and promotes latency in primary CD4+ infected T cells. Interestingly, ATF1 regulates CCR5 expression and indirectly affects R5-tropic HIV infection. Mechanistically, ATF1 depletion impairs occupancy of RNA Polymerase II on the HIV promoter, and this is accompanied with elevated levels of H3K9me3 repression histone mark around the viral promoter. Genome wide analysis of ATF1 shows that it occupies cellular gene promoters including HIV, thereby controls gene targets that indirectly affect HIV infection. We conclude that ATF1 is an activator of gene transcription that dictates HIV gene expression via both direct and indirect mechanisms.
2025-07-02 | GSE286022 | GEO
Project description:The question of how HIV-1 interfaces with cellular microRNA (miRNA) biogenesis and effector mechanisms has been highly controversial. Here, we first used deep sequencing of small RNAs present in two different infected cell lines (TZM-bl and C8166) and two types of primary human cells (CD4+ PBMCs and macrophages) to unequivocally demonstrate that HIV-1 does not encode any viral miRNAs. Perhaps surprisingly, we also observed that infection of T cells by HIV-1 has only a modest effect on the expression of cellular miRNAs at early times after infection. Comprehensive analysis of miRNA binding to the HIV-1 genome using the photoactivatable ribonucleoside-induced crosslinking and immunoprecipitation (PAR-CLIP) technique revealed several binding sites for cellular miRNAs, a subset of which were shown to be capable of mediating miRNA-mediated repression of gene expression. However, the main finding from this analysis is that HIV-1 transcripts are largely refractory to miRNA binding, most probably due to extensive viral RNA secondary structure. Together, these data demonstrate that HIV-1 neither encodes viral miRNAs nor strongly influences cellular miRNA expression, at least early after infection, and imply that HIV-1 transcripts have evolved to avoid inhibition by pre-existing cellular miRNAs by adopting extensive RNA secondary structures that occlude most potential miRNA binding sites.
2014-07-31 | GSE59944 | GEO
Project description:The epigenetic mechanisms established by histone modifications may affect the transcriptional silencing of HIV-1 and viral latency. A systematic epigenome profiling could be applicable to develop new epigenetic diagnostic markers for detecting HIV-1 latency. In this study, histone modification profiles of HIV-1 latency cell lines were compared with those of uninfected CD4+ T cell line. The HIV-1 latency gave rise to differential histone modification regions. The differential enrichment patterns helped us to define potential effector genes leading to the viral latency. The histone H3K4me3 and H3K9ac profiles were obtained from the HIV-1 latency cell lines (NCHA1, NCHA2, and ACH2) and control CD4+ T cell line (A3.01)
2014-06-06 | E-GEOD-58247 | biostudies-arrayexpress
Project description:Despite effective antiretroviral therapy (ART), HIV-1 persists as an integrated DNA provirus in the genome of infected cells. Host cells can regulate HIV-1 transcription at the HIV-1 integration site dependent on the location (actively transcribed genes vs repressive chromatin) and the orientation (in the same vs opposite orientation of the host gene transcription) of HIV-1 integration. Presumably, HIV-1 follows the host gene transcriptional activity at the HIV-1 integration site. We interrogated HIV-1-host gene transcriptional interactions at the HIV-1 integration site using CRISPR-mediated activation and inhibition of the host genes (in which HIV-1 was integrated) in seven HIV-1-infected Jurkat T cell clones with known HIV-1 integration sites in the introns of actively transcribed genes and a non-genic region. Using ATAC-seq and strand-specific RNA-seq to examine chromatin accessibility and RNA transcription levels, we found that host gene activation did not increase HIV-1 transcription, while host gene inhibition did not decrease HIV-1 transcription. HIV-1 drove high levels of aberrant host RNA transcription regardless of the HIV-1 integration orientation. HIV-1-driven aberrant host RNA transcription was inhibited by CRISPR-mediated HIV-1 inhibition but not by CRISPR-mediated host gene activation or inhibition. When HIV-1 was integrated into a non-genic region, HIV-1 increased host chromatin accessibility and drove high levels of aberrant host RNA transcription. Overall, HIV-1 LTR promoter-driven transcriptional activity dominated over the host promoter activity. HIV-1 transcription does not passively follow host gene activity. Our results highlight that despite effective ART, silencing HIV-1 promoter is required to inhibit HIV-1-driven aberrant host gene expression and chronic immune activation.
2025-10-21 | GSE302221 | GEO