ArticlePLoS pathogens2019
Effector memory differentiation increases detection of replication-competent HIV-l in resting CD4+ T cells from virally suppressed individuals.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
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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.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- MVA.HIVconsvX vaccination-evoked T cell expansion inversely associates with age in people with HIV-1 on antiretroviral therapy.The Journal of clinical investigation · 2026Trial
- Comparison of manual and automated ultrasensitive assays for residual HIV-1 in plasma from individuals on suppressive antiretroviral therapy.Journal of clinical microbiology · 2025Article
- Mild HIV-specific selective forces overlaying natural CD4+ T cell dynamics explain the clonality and decay dynamics of HIV reservoir cells.Cell systems · 2025Article
- Applications and limitations of the passenger hypothesis for HIV reservoir persistence and cure.Journal of virology · 2025Review
- Phenotyping Viral Reservoirs to Reveal HIV-1 Hiding Places.Current HIV/AIDS reports · 2025Review
- Double, double toil and trouble: transforming growth factor beta (TGF-β) in HIV infection.Frontiers in immunology · 2025Review
- Measuring Human Immunodeficiency Virus Reservoirs: Do We Need to Choose Between Quantity and Quality?The Journal of infectious diseases · 2024Review
- Article
- Examining Chronic Inflammation, Immune Metabolism, and T Cell Dysfunction in HIV Infection.Viruses · 2024Review
- A histone deacetylase network regulates epigenetic reprogramming and viral silencing in HIV-infected cells.Cell chemical biology · 2023Article
- Estimating the contribution of CD4 T cell subset proliferation and differentiation to HIV persistence.Nature communications · 2023Article
- Application of ultrasensitive digital ELISA for p24 enables improved evaluation of HIV-1 reservoir diversity and growth kinetics in viral outgrowth assays.Scientific reports · 2023Article
- Use of laboratory-developed assays in global HIV-1 treatment-monitoring and research.Scientific reports · 2023Review
- Transient T Cell Expansion, Activation, and Proliferation in Therapeutically Vaccinated Simian Immunodeficiency Virus-Positive Macaques Treated with N-803.Journal of virology · 2022Article
- Heterogeneity of Latency Establishment in the Different Human CD4Journal of virology · 2022Article
- Article
- Article
- The reservoir of latent HIV.Frontiers in cellular and infection microbiology · 2022Review
- Ex Vivo Differentiation of Resting CD4+ T Lymphocytes Enhances Detection of Replication Competent HIV-1 in Viral Outgrowth Assays.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Quantification of Total HIV DNA as a Marker to Measure Viral Reservoir: Methods and Potential Implications for Clinical Practice.Diagnostics (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Studies have demonstrated that intensive ART alone is not capable of eradicating HIV-1, as the virus rebounds within a few weeks upon treatment interruption. Viral rebound may be induced from several cellular subsets; however, the majority of proviral DNA has been found in antigen experienced resting CD4+ T cells. To achieve a cure for HIV-1, eradication strategies depend upon both understanding mechanisms that drive HIV-1 persistence as well as sensitive assays to measure the frequency of infected cells after therapeutic interventions. Assays such as the quantitative viral outgrowth assay (QVOA) measure HIV-1 persistence during ART by ex vivo activation of resting CD4+ T cells to induce latency reversal; however, recent studies have shown that only a fraction of replication-competent viruses are inducible by primary mitogen stimulation. Previous studies have shown a correlation between the acquisition of effector memory phenotype and HIV-1 latency reversal in quiescent CD4+ T cell subsets that harbor the reservoir. Here, we apply our mechanistic understanding that differentiation into effector memory CD4+ T cells more effectively promotes HIV-1 latency reversal to significantly improve proviral measurements in the QVOA, termed differentiation QVOA (dQVOA), which reveals a significantly higher frequency of the inducible HIV-1 replication-competent reservoir in resting CD4+ T 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.