ArticlePLoS pathogens2015
Modeling the Effects of Vorinostat In Vivo Reveals both Transient and Delayed HIV Transcriptional Activation and Minimal Killing of Latently Infected Cells.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- AZD5582 robustly reactivates latently infected cells and clears the majority of those reactivated from the SIV reservoir.bioRxiv : the preprint server for biology · 2026Article
- Evaluating the long-term effects of combination antiretroviral therapy of HIV infection: a modeling study.Journal of mathematical biology · 2025Article
- Modelling HIV-1 control and remission.NPJ systems biology and applications · 2024Review
- Deciphering the similarities and disparities of molecular mechanisms behind respiratory epithelium response to HCoV-229E and SARS-CoV-2 and drug repurposing, a systems biology approach.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024Article
- Anti-Cryptosporidial Drug-Discovery Challenges and Existing Therapeutic Avenues: A "One-Health" Concern.Life (Basel, Switzerland) · 2024Review
- Venetoclax, alone and in combination with the BH3 mimetic S63845, depletes HIV-1 latently infected cells and delays rebound in humanized mice.Cell reports. Medicine · 2023Article
- PARP1 Might Substitute HSF1 to Reactivate Latent HIV-1 by Binding to Heat Shock Element.Cells · 2022Article
- Pharmacology of HIV Cure: Site of Action.Clinical pharmacology and therapeutics · 2021Review
- Challenges and Promise of Human Immunodeficiency Virus Remission.The Journal of infectious diseases · 2021Review
- The Potential Contribution of Caveolin 1 to HIV Latent Infection.Pathogens (Basel, Switzerland) · 2020Review
- BCL-2 antagonism sensitizes cytotoxic T cell-resistant HIV reservoirs to elimination ex vivo.The Journal of clinical investigation · 2020Article
- Differences in Transcriptional Dynamics Between T-cells and Macrophages as Determined by a Three-State Mathematical Model.Scientific reports · 2020Article
- Leveraging Computational Modeling to Understand Infectious Diseases.Current pathobiology reports · 2020Review
- Predictions of time to HIV viral rebound following ART suspension that incorporate personal biomarkers.PLoS computational biology · 2019Article
- Have Cells Harboring the HIV Reservoir Been Immunoedited?Frontiers in immunology · 2019Article
- Epigenetics in Sepsis: Understanding Its Role in Endothelial Dysfunction, Immunosuppression, and Potential Therapeutics.Frontiers in immunology · 2019Review
- Probabilistic control of HIV latency and transactivation by the Tat gene circuit.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Determinants of the efficacy of HIV latency-reversing agents and implications for drug and treatment design.JCI insight · 2018Article
- Variation in cell-associated unspliced HIV RNA on antiretroviral therapy is associated with the circadian regulator brain-and-muscle-ARNT-like-1.AIDS (London, England) · 2018Observational
- Barriers for HIV Cure: The Latent Reservoir.AIDS research and human retroviruses · 2018Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Recent efforts to cure human immunodeficiency virus type-1 (HIV-1) infection have focused on developing latency reversing agents as a first step to eradicate the latent reservoir. The histone deacetylase inhibitor, vorinostat, has been shown to activate HIV RNA transcription in CD4+ T-cells and alter host cell gene transcription in HIV-infected individuals on antiretroviral therapy. In order to understand how latently infected cells respond dynamically to vorinostat treatment and determine the impact of vorinostat on reservoir size in vivo, we have constructed viral dynamic models of latency that incorporate vorinostat treatment. We fitted these models to data collected from a recent clinical trial in which vorinostat was administered daily for 14 days to HIV-infected individuals on suppressive ART. The results show that HIV transcription is increased transiently during the first few hours or days of treatment and that there is a delay before a sustained increase of HIV transcription, whose duration varies among study participants and may depend on the long term impact of vorinostat on host gene expression. Parameter estimation suggests that in latently infected cells, HIV transcription induced by vorinostat occurs at lower levels than in productively infected cells. Furthermore, the estimated loss rate of transcriptionally induced cells remains close to baseline in most study participants, suggesting vorinostat treatment does not induce latently infected cell killing and thus reduce the latent reservoir in vivo.
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