ArticleRetrovirology2019
Heterogeneity in HIV and cellular transcription profiles in cell line models of latent and productive infection: implications for HIV latency.
Article in Retrovirology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it.
- HIV-1 Infection Transcriptomics: Meta-Analysis of CD4+ T Cells Gene Expression Profiles.Viruses · 2021Pooled it
- The BAF complex inhibitor pyrimethamine reverses HIV-1 latency in people with HIV-1 on antiretroviral therapy.Science advances · 2023Trial
- Selection of effective LRAs using a newly designedMicrobiology spectrum · 2026Article
- Review
- USP45-mediated deubiquitination of HIV-1 Tat regulates viral transcription and latency.Frontiers in microbiology · 2026Article
- Distinct roles of dopamine receptors in HIV latency reversal in a myeloid cell model.Frontiers in immunology · 2026Article
- Using single cell technologies to understand HIV latency models.Current opinion in HIV and AIDS · 2025Review
- Anti-HIV-1 HSPC-based gene therapy with safety kill switch to defend against and attack HIV-1 infection.Molecular therapy. Methods & clinical development · 2025Article
- Integrator complex subunit 12 knockout overcomes a transcriptional block to HIV latency reversal.eLife · 2025Article
- Nuclear retention of unspliced HIV-1 RNA as a reversible post-transcriptional block in latency.Nature communications · 2025Article
- Review
- Article
- Review
- Single-molecule RNA-FISH analysis reveals stochasticity in reactivation of latent HIV-1 regulated by Nuclear Orphan Receptors NR4A and cMYC.Research square · 2024Article
- Targeting Viral Transcription for HIV Cure Strategies.Microorganisms · 2024Review
- Article
- Gesicles packaging dCas9-VPR ribonucleoprotein complexes can combine with vorinostat and promote HIV proviral transcription.Molecular therapy. Methods & clinical development · 2024Article
- Targeted shock-and-kill HIV-1 gene therapy approach combining CRISPR activation, suicide gene tBid and retargeted adenovirus delivery.Gene therapy · 2024Article
- Direct Analysis of HIV mRNA mMethods in molecular biology (Clifton, N.J.) · 2024Article
- Lipid nanocarrier targeting activated macrophages for antiretroviral therapy of HIV reservoir.Nanomedicine (London, England) · 2023Article
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Authors and funding
11 authors.
Funding
Abstract
backgroundHIV-infected cell lines are widely used to study latent HIV infection, which is considered the main barrier to HIV cure. We hypothesized that these cell lines differ from each other and from cells from HIV-infected individuals in the mechanisms underlying latency.
resultsTo quantify the degree to which HIV expression is inhibited by blocks at different stages of HIV transcription, we employed a recently-described panel of RT-ddPCR assays to measure levels of 7 HIV transcripts ("read-through," initiated, 5' elongated, mid-transcribed/unspliced [Pol], distal-transcribed [Nef], polyadenylated, and multiply-sliced [Tat-Rev]) in bulk populations of latently-infected (U1, ACH-2, J-Lat) and productively-infected (8E5, activated J-Lat) cell lines. To assess single-cell variation and investigate cellular genes associated with HIV transcriptional blocks, we developed a novel multiplex qPCR panel and quantified single cell levels of 7 HIV targets and 89 cellular transcripts in latently- and productively-infected cell lines. The bulk cell HIV transcription profile differed dramatically between cell lines and cells from ART-suppressed individuals. Compared to cells from ART-suppressed individuals, latent cell lines showed lower levels of HIV transcriptional initiation and higher levels of polyadenylation and splicing. ACH-2 and J-Lat cells showed different forms of transcriptional interference, while U1 cells showed a block to elongation. Single-cell studies revealed marked variation between/within cell lines in expression of HIV transcripts, T cell phenotypic markers, antiviral factors, and genes implicated in latency. Expression of multiply-spliced HIV Tat-Rev was associated with expression of cellular genes involved in activation, tissue retention, T cell transcription, and apoptosis/survival.
conclusionsHIV-infected cell lines differ from each other and from cells from ART-treated individuals in the mechanisms governing latent HIV infection. These differences in viral and cellular gene expression must be considered when gauging the suitability of a given cell line for future research on HIV. At the same time, some features were shared across cell lines, such as low expression of antiviral defense genes and a relationship between productive infection and genes involved in survival. These features may contribute to HIV latency or persistence in vivo, and deserve further study using novel single cell assays such as those described in this manuscript.
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