ArticleJournal of virology2011
Influence of host gene transcription level and orientation on HIV-1 latency in a primary-cell model.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed.
- Intact HIV-1 proviruses accumulate at distinct chromosomal positions during prolonged antiretroviral therapy.The Journal of clinical investigation · 2019Trial
- Antigen Stimulation Reactivates HIV-1 Proviruses Despite Integration in Repressive Chromatin.bioRxiv : the preprint server for biology · 2026Article
- Article
- The Complex Interactions Between HIV-1 and Human Host Cell Genome: From Molecular Mechanisms to Clinical Practice.International journal of molecular sciences · 2025Review
- CD4+ T cells with latent HIV-1 have reduced proliferative responses to T cell receptor stimulation.The Journal of experimental medicine · 2024Article
- Establishment, Persistence, and Reactivation of Latent HIV-1 Infection in Renal Epithelial Cells.Journal of virology · 2022Article
- HIV-1 integration sites in CD4+ T cells during primary, chronic, and late presentation of HIV-1 infection.JCI insight · 2021Article
- Factors that mold the nuclear landscape of HIV-1 integration.Nucleic acids research · 2021Review
- Review
- The chromatin landscape at the HIV-1 provirus integration site determines viral expression.Nucleic acids research · 2020Article
- Article
- Differences in inducibility of the latent HIV reservoir in perinatal and adult infection.JCI insight · 2020Article
- Novel pathways of HIV latency reactivation revealed by integrated analysis of transcriptome and target profile of bryostatin.Scientific reports · 2020Article
- The forces driving clonal expansion of the HIV-1 latent reservoir.Virology journal · 2020Review
- Article
- Effect of transcription inhibition and generation of suppressive viral non-coding RNAs.Retrovirology · 2019Article
- Tat inhibition by didehydro-Cortistatin A promotes heterochromatin formation at the HIV-1 long terminal repeat.Epigenetics & chromatin · 2019Article
- Roles of CDKs in RNA polymerase II transcription of the HIV-1 genome.Transcription · 2019Review
- ISDB: a database toolkit for storing and analyzing viral integration site data.Bioinformatics (Oxford, England) · 2019Article
- Establishment of a Novel Humanized Mouse Model To InvestigateJournal of virology · 2019Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Human immunodeficiency virus type 1 (HIV-1) establishes a latent reservoir in resting memory CD4(+) T cells. This latent reservoir is a major barrier to the eradication of HIV-1 in infected individuals and is not affected by highly active antiretroviral therapy (HAART). Reactivation of latent HIV-1 is a possible strategy for elimination of this reservoir. The mechanisms with which latency is maintained are unclear. In the analysis of the regulation of HIV-1 gene expression, it is important to consider the nature of HIV-1 integration sites. In this study, we analyzed the integration and transcription of latent HIV-1 in a primary CD4(+) T cell model of latency. The majority of integration sites in latently infected cells were in introns of transcription units. Serial analysis of gene expression (SAGE) demonstrated that more than 90% of those host genes harboring a latent integrated provirus were transcriptionally active, mostly at high levels. For latently infected cells, we observed a modest preference for integration in the same transcriptional orientation as the host gene (63.8% versus 36.2%). In contrast, this orientation preference was not observed in acutely infected or persistently infected cells. These results suggest that transcriptional interference may be one of the important factors in the establishment and maintenance of HIV-1 latency. Our findings suggest that disrupting the negative control of HIV-1 transcription by upstream host promoters could facilitate the reactivation of latent HIV-1 in some resting CD4(+) T cells.
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