Trial reportPLoS pathogens2017
Treatment with integrase inhibitor suggests a new interpretation of HIV RNA decay curves that reveals a subset of cells with slow integration.
Trial report in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 60 citations in OpenAlex.
- Dolutegravir/Abacavir/Lamivudine in Acute HIV-1 Results in Rapid Suppression and Restoration of CD4 T-cell Subsets Without Accelerated Decay of Latent HIV-1.Open forum infectious diseases · 2025Trial
- Modeling quantifies in vivo neutralization, Fc-mediated killing, and resistance in human clinical trials of five anti-HIV broadly neutralizing antibodies.bioRxiv : the preprint server for biology · 2026Article
- Clinical trial simulation of antiviral drugs.Journal of virology · 2026Review
- The decay of HIV under anti-retroviral therapy is biphasic even in humanized mice with just T cells.Journal of virology · 2026Article
- Intact HIV DNA decays in children with and without complete viral load suppression.PLoS pathogens · 2025Article
- Latent reservoirs in memory T cell subsets are linked to poor immune recovery in people living with HIV.Frontiers in immunology · 2025Article
- SIV Env RhmAbs + N-803 at ART initiation prolongs viral decay without disrupting reservoir establishment in SIV-infected infant macaques.PLoS pathogens · 2025Article
- A consensus mathematical model of vaccine-induced antibody dynamics for multiple vaccine platforms and pathogens.Frontiers in immunology · 2025Article
- Assessing advances in three decades of clinical antiretroviral therapy on the HIV-1 reservoir.The Journal of clinical investigation · 2024Article
- Dominant CD4Cell reports. Medicine · 2023Article
- CD8Nature communications · 2023Article
- Mathematical modeling indicates that regulatory inhibition of CD8+ T cell cytotoxicity can limit efficacy of IL-15 immunotherapy in cases of high pre-treatment SIV viral load.PLoS computational biology · 2023Article
- DNA ultra-sensitive quantification, a technology for studying HIV unintegrated linear DNA.Cell reports methods · 2023Article
- A simple model for viral decay dynamics and the distribution of infected cell life spans in SHIV-infected infant rhesus macaques.Mathematical biosciences · 2023Article
- Complex decay dynamics of HIV virions, intact and defective proviruses, and 2LTR circles following initiation of antiretroviral therapy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Estimation of the in vivo neutralization potency of eCD4Ig and conditions for AAV-mediated production for SHIV long-term remission.Science advances · 2022Article
- Review
- Mathematical modeling of N-803 treatment in SIV-infected non-human primates.PLoS computational biology · 2021Article
- Mechanistic basis of post-treatment control of SIV after anti-α4β7 antibody therapy.PLoS computational biology · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
The kinetics of HIV-1 decay under treatment depends on the class of antiretrovirals used. Mathematical models are useful to interpret the different profiles, providing quantitative information about the kinetics of virus replication and the cell populations contributing to viral decay. We modeled proviral integration in short- and long-lived infected cells to compare viral kinetics under treatment with and without the integrase inhibitor raltegravir (RAL). We fitted the model to data obtained from participants treated with RAL-containing regimes or with a four-drug regimen of protease and reverse transcriptase inhibitors. Our model explains the existence and quantifies the three phases of HIV-1 RNA decay in RAL-based regimens vs. the two phases observed in therapies without RAL. Our findings indicate that HIV-1 infection is mostly sustained by short-lived infected cells with fast integration and a short viral production period, and by long-lived infected cells with slow integration but an equally short viral production period. We propose that these cells represent activated and resting infected CD4+ T-cells, respectively, and estimate that infection of resting cells represent ~4% of productive reverse transcription events in chronic infection. RAL reveals the kinetics of proviral integration, showing that in short-lived cells the pre-integration population has a half-life of ~7 hours, whereas in long-lived cells this half-life is ~6 weeks. We also show that the efficacy of RAL can be estimated by the difference in viral load at the start of the second phase in protocols with and without RAL. Overall, we provide a mechanistic model of viral infection that parsimoniously explains the kinetics of viral load decline under multiple classes of antiretrovirals.
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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 Socratic graph.