ReviewCurrent opinion in HIV and AIDS2018
HIV integration sites and implications for maintenance of the reservoir.
Review in Current opinion in HIV and AIDS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 42 citations in OpenAlex.
- The LEDGIN GS-9822 inhibits HIV-2 infection and enhances HIV-2 latency.Microbiology spectrum · 2026Article
- HIV-1 Integration Site Determines the Transcriptional Fate and Persistence of Integrated Proviruses.bioRxiv : the preprint server for biology · 2026Article
- Clonal heterogeneity and antigenic stimulation shape persistence of the latent reservoir of HIV.PLoS computational biology · 2025Article
- Advancements in single-cell techniques for examining the HIV reservoir: pathways to a cure.mBio · 2025Review
- Synergistic Activity of Second Mitochondrial-Derived Activator of Caspases Mimetic with Toll-like Receptor 8 Agonist Reverses HIV-1-Latency and Enhances Antiviral Immunity.International journal of molecular sciences · 2025Article
- Promotion of HIV clearance by sensitization of HIV reservoirs to cell death.Frontiers in immunology · 2025Article
- SIV infection and ARV treatment reshape the transcriptional and epigenetic profile of naïve and memory T cellsJournal of virology · 2024Article
- The HIV-2 OGH double reporter virus shows that HIV-2 is less cytotoxic and less sensitive to reactivation from latency than HIV-1 in cell culture.Journal of virus eradication · 2023Article
- HIV Reservoir: How to Measure It?Current HIV/AIDS reports · 2023Review
- Antiretroviral APOBEC3 cytidine deaminases alter HIV-1 provirus integration site profiles.Nature communications · 2023Article
- Article
- Genome-wide associated variants of subclinical atherosclerosis among young people with HIV and gene-environment interactions.Journal of translational medicine · 2022Article
- Intact provirus and integration sites analysis in acute HIV-1 infection and changes after one year of early antiviral therapy.Journal of virus eradication · 2022Article
- Article
- Droplet-microfluidics-assisted sequencing of HIV proviruses and their integration sites in cells from people on antiretroviral therapy.Nature biomedical engineering · 2022Article
- The reservoir of latent HIV.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Review
- Towards a Functional Cure of HIV-1: Insight Into the Chromatin Landscape of the Provirus.Frontiers in microbiology · 2021Review
- Block-And-Lock: New Horizons for a Cure for HIV-1.Viruses · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
purpose of reviewTo provide an overview of recent research of how HIV integration relates to productive and latent infection and implications for cure strategies. RECENT
findingsHow and where HIV integrates provides new insights into how HIV persists on antiretroviral therapy (ART). Clonal expansion of infected cells with the same integration site demonstrates that T-cell proliferation is an important factor in HIV persistence, however, the driver of proliferation remains unclear. Clones with identical integration sites harbouring defective provirus can accumulate in HIV-infected individuals on ART and defective proviruses can express RNA and produce protein. HIV integration sites differ in clonally expanded and nonexpanded cells and in latently and productively infected cells and this influences basal and inducible transcription. There is a growing number of cellular proteins that can alter the pattern of integration to favour latency. Understanding these pathways may identify new interventions to eliminate latently infected cells. SUMMARY: Using advances in analysing HIV integration sites, T-cell proliferation of latently infected cells is thought to play a major role in HIV persistence. Clonal expansion has been demonstrated with both defective and intact viruses. Production of viral RNA and protein from defective viruses may play a role in driving chronic immune activation. The site of integration may determine the likelihood of proliferation and the degree of basal and induced transcription. Finally, host factors and gene expression at the time of infection may determine the integration site. Together these new insights may lead to novel approaches to elimination of latently infected cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.