ArticleRetrovirology2017
HIV integration sites in latently infected cell lines: evidence of ongoing replication.
Article in Retrovirology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 80 citations in OpenAlex.
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- In vitro HIV DNA integration in STAT3 drives T cell persistence-A model of HIV-associated T cell lymphoma.PLoS pathogens · 2025Article
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- KDM5A/B contribute to HIV-1 latent infection and survival of HIV-1 infected cells.Antiviral research · 2024Article
- Nanoparticle delivery of Tat synergizes with classical latency reversal agents to express HIV antigen targets.Antimicrobial agents and chemotherapy · 2024Article
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- Advancing towards HIV-1 remission: Insights and innovations in stem cell therapies.Archives of stem cell and therapy · 2024Article
- Long Noncoding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Promotes HIV-1 Replication through Modulating microRNAs in Macrophages.Journal of virology · 2023Article
- Strategic self-limiting production of infectious HIV particles by CRISPR in permissive cells.Molecular therapy. Nucleic acids · 2023Article
- Controversies in the Design of Strategies for the Cure of HIV Infection.Pathogens (Basel, Switzerland) · 2023Review
- Epigenetic Regulation of HIV-1 Sense and Antisense Transcription in Response to Latency-Reversing Agents.Non-coding RNA · 2023Article
- HIV integration in the human brain is linked to microglial activation and 3D genome remodeling.Molecular cell · 2022Article
- Adaptation to HLA-associated immune pressure over the course of HIV infection and in circulating HIV-1 strains.PLoS pathogens · 2022Article
- Blockade of TGF-β signaling reactivates HIV-1/SIV reservoirs and immune responses in vivo.JCI insight · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundAssessing the location and frequency of HIV integration sites in latently infected cells can potentially inform our understanding of how HIV persists during combination antiretroviral therapy. We developed a novel high throughput sequencing method to evaluate HIV integration sites in latently infected cell lines to determine whether there was virus replication or clonal expansion in these cell lines observed as multiple integration events at the same position.
resultsWe modified a previously reported method using random DNA shearing and PCR to allow for high throughput robotic processing to identify the site and frequency of HIV integration in latently infected cell lines. Latently infected cell lines infected with intact virus demonstrated multiple distinct HIV integration sites (28 different sites in U1, 110 in ACH-2 and 117 in J1.1 per 150,000 cells). In contrast, cell lines infected with replication-incompetent viruses (J-Lat cells) demonstrated single integration sites. Following in vitro passaging of the ACH-2 cell line, we observed a significant increase in the frequency of unique HIV integration sites and there were multiple mutations and large deletions in the proviral DNA. When the ACH-2 cell line was cultured with the integrase inhibitor raltegravir, there was a significant decrease in the number of unique HIV integration sites and a transient increase in the frequency of 2-LTR circles consistent with virus replication in these cells.
conclusionCell lines latently infected with intact HIV demonstrated multiple unique HIV integration sites indicating that these cell lines are not clonal and in the ACH-2 cell line there was evidence of low level virus replication. These findings have implications for the use of latently infected cell lines as models of HIV latency and for the use of these cells as standards.
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