ReviewCell host & microbe2016
What Integration Sites Tell Us about HIV Persistence.
Review in Cell host & microbe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 70 citations in OpenAlex.
- Selective persistence of HIV-1-infected T cell clones can occur through immune reprogramming driven by defective, transcriptionally active proviruses.PLoS pathogens · 2026Article
- Antigen Stimulation Reactivates HIV-1 Proviruses Despite Integration in Repressive Chromatin.bioRxiv : the preprint server for biology · 2026Article
- AZD5582 robustly reactivates latently infected cells and clears the majority of those reactivated from the SIV reservoir.bioRxiv : the preprint server for biology · 2026Article
- Development and Evaluation of a Novel Relatively Low-Cost Method to Derive HIV-1 Integration Sites and Proviral Sequences.Viruses · 2026Article
- HIV-1 Integration Site Determines the Transcriptional Fate and Persistence of Integrated Proviruses.bioRxiv : the preprint server for biology · 2026Article
- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
- Comparing acute versus AIDS ART initiation on HIV-1 integration sites and clonal expansion.Signal transduction and targeted therapy · 2025Article
- The Assessment of Knowledge About Cervical Cancer, HPV Vaccinations, and Screening Programs Among Women as an Element of Cervical Cancer Prevention in Poland.Journal of personalized medicine · 2024Article
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- Dynamic modulation of the non-canonical NF-κB signaling pathway for HIV shock and kill.Frontiers in cellular and infection microbiology · 2024Review
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- Decoding Human Genome Regulatory Features That Influence HIV-1 Proviral Expression and Fate Through an Integrated Genomics Approach.Bioinformatics and biology insights · 2022Article
- Review
- Review
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- Mouse papillomavirus type 1 (MmuPV1) DNA is frequently integrated in benign tumors by microhomology-mediated end-joining.PLoS pathogens · 2021Article
- rigrag: high-resolution mapping of genic targeting preferences during HIV-1 integration in vitro and in vivo.Nucleic acids research · 2021Article
- Article
- Integration in oncogenes plays only a minor role in determining the in vivo distribution of HIV integration sites before or during suppressive antiretroviral therapy.PLoS pathogens · 2021Article
- Increased Proviral DNA in Circulating Cells Correlates with Plasma Viral Rebound in Simian Immunodeficiency Virus-Infected Rhesus Macaques after Antiretroviral Therapy Interruption.Journal of virology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Advances in technology have made it possible to analyze integration sites in cells from HIV-infected patients. A significant fraction of infected cells in patients on long-term therapy are clonally expanded; in some cases the integrated viral DNA contributes to the clonal expansion of the infected cells. Although the large majority (>95%) of the HIV proviruses in treated patients are defective, expanded clones can carry replication-competent proviruses, and cells from these clones can release infectious virus. As discussed in this Perspective, it is likely that cells that produce virus are strongly selected against in vivo, and cells with replication competent proviruses expand and survive because only a small fraction of the cells produce virus. These findings have implications for strategies that are intended to eliminate the reservoir of infected cells that has made it almost impossible to cure HIV-infected patients.
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What OpenQuestion holds
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.