ArticleRetrovirology2016
In vivo analysis of the effect of panobinostat on cell-associated HIV RNA and DNA levels and latent HIV infection.
Article in Retrovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 67 citations in OpenAlex.
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- Breaking into HIV-1's Epigenetic Vault: Cure Strategies to Eliminate the Viral Reservoir.Viruses · 2026Review
- Traditional Medicine Extracts ofInternational journal of molecular sciences · 2026Article
- Identification of inducible HIV reservoirs in tonsillar, intestinal and cervical tissue models of HIV latency.Nature communications · 2025Article
- NK cell immunotherapy administered at the time of HIV recrudescence is associated with viral control.bioRxiv : the preprint server for biology · 2025Article
- Humanized DRAGA mice are a valuable model to study novel immunotherapies for HIV-1.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- A TCR-mimic bispecific antibody reduces HIV-1 provirus and delays viral rebound in HLA-matched humanized mice.bioRxiv : the preprint server for biology · 2025Article
- Impacts of immune checkpoint inhibitors use on the HIV reservoir are linked to provirus sequences but not integration sites.Scientific reports · 2025Article
- HIV-1 latency reversal agent boosting is not limited by opioid use.JCI insight · 2024Article
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- Nanoparticle delivery of Tat synergizes with classical latency reversal agents to express HIV antigen targets.Antimicrobial agents and chemotherapy · 2024Article
- HIV-1 latency reversal agent boosting is not limited by opioid use.medRxiv : the preprint server for health sciences · 2024Article
- The Humanized Mouse Model: What Added Value Does It Offer for HIV Research?Pathogens (Basel, Switzerland) · 2023Review
- Generation of functional human T cell development in NOD/SCID/IL2rγStem cell reports · 2023Article
- Bromodomain and Extra-Terminal Inhibitor BMS-986158 Reverses Latent HIV-1 Infection In Vitro and Ex Vivo by Increasing CDK9 Phosphorylation and Recruitment.Pharmaceuticals (Basel, Switzerland) · 2022Article
- So Pathogenic or So What?-A Brief Overview of SIV Pathogenesis with an Emphasis on Cure Research.Viruses · 2022Review
- Human Hematopoietic Stem Cell (HSC)-Engrafted NSG Mice for HIV Latency Research.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Histone deacetylase inhibition reduces deleterious cytokine release induced by ingenol stimulation.Biochemical pharmacology · 2022Article
- Inducing Long-Term HIV-1 Latency in the TKO-BLT Mouse Model.Methods in molecular biology (Clifton, N.J.) · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe latent reservoir in resting CD4(+) T cells presents a major barrier to HIV cure. Latency-reversing agents are therefore being developed with the ultimate goal of disrupting the latent state, resulting in induction of HIV expression and clearance of infected cells. Histone deacetylase inhibitors (HDACi) have received a significant amount of attention for their potential as latency-reversing agents.
resultsHere, we have investigated the in vitro and systemic in vivo effect of panobinostat, a clinically relevant HDACi, on HIV latency. We showed that panobinostat induces histone acetylation in human PBMCs. Further, we showed that panobinostat induced HIV RNA expression and allowed the outgrowth of replication-competent virus ex vivo from resting CD4(+) T cells of HIV-infected patients on suppressive antiretroviral therapy (ART). Next, we demonstrated that panobinostat induced systemic histone acetylation in vivo in the tissues of BLT humanized mice. Finally, in HIV-infected, ART-suppressed BLT mice, we evaluated the effect of panobinostat on systemic cell-associated HIV RNA and DNA levels and the total frequency of latently infected resting CD4(+) T cells. Our data indicate that panobinostat treatment resulted in systemic increases in cellular levels of histone acetylation, a key biomarker for in vivo activity. However, panobinostat did not affect the levels of cell-associated HIV RNA, HIV DNA, or latently infected resting CD4(+) T cells.
conclusionWe have demonstrated robust levels of systemic histone acetylation after panobinostat treatment of BLT humanized mice; and we did not observe a detectable change in the levels of cell-associated HIV RNA, HIV DNA, or latently infected resting CD4(+) T cells in HIV-infected, ART-suppressed BLT mice. These results are consistent with the modest effects noted in vitro and suggest that combination therapies may be necessary to reverse latency and enable clearance. Animal models will contribute to the progress towards an HIV cure.
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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.