ArticleJournal of virology2017
Maintenance of the HIV Reservoir Is Antagonized by Selective BCL2 Inhibition.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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.
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Who cites it
49 citing papers in PubMed, 72 citations in OpenAlex.
- Randomized Trial of Ruxolitinib in Antiretroviral-Treated Adults With Human Immunodeficiency Virus.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Trial
- Cytotoxic CD4 T Cells: Dual Agents in HIV-1 Pathogenesis and Persistence.Current HIV/AIDS reports · 2026Review
- Resist to persist: resistance of the HIV reservoir to immune-mediated clearance.Current opinion in HIV and AIDS · 2025Review
- Host-directed approaches in the pursuit of a cure for HIV.Antiviral research · 2025Review
- Immune-mediated strategies to solving the HIV reservoir problem.Nature reviews. Immunology · 2025Review
- ABT-263, a BCL-2 inhibitor, selectively eliminates latently HIV-1-infected cells without viral reactivation.PloS one · 2025Article
- Article
- Isotretinoin promotes elimination of translation-competent HIV latent reservoirs in CD4T cells.PLoS pathogens · 2024Article
- Emerging roles of senolytics/senomorphics in HIV-related co-morbidities.Biochemical pharmacology · 2024Review
- Microglia and macrophages alterations in the CNS during acute SIV infection: A single-cell analysis in rhesus macaques.PLoS pathogens · 2024Article
- Microglia and macrophages alterations in the CNS during acute SIV infection: a single-cell analysis in rhesus macaques.bioRxiv : the preprint server for biology · 2024Article
- Defining the Effects of PKC Modulator HIV Latency-Reversing Agents on Natural Killer Cells.Pathogens & immunity · 2024Article
- 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
- Article
- Potential Role of Polyphenolic Flavonoids as Senotherapeutic Agents in Degenerative Diseases and Geroprotection.Pharmaceutical medicine · 2022Review
- Senotherapeutics in Cancer and HIV.Cells · 2022Review
- Biological ageing with HIV infection: evaluating the geroscience hypothesis.The lancet. Healthy longevity · 2022Article
- So Pathogenic or So What?-A Brief Overview of SIV Pathogenesis with an Emphasis on Cure Research.Viruses · 2022Review
- Repurposing BCL-2 and Jak 1/2 inhibitors: Cure and treatment of HIV-1 and other viral infections.Frontiers in immunology · 2022Review
- The reservoir of latent HIV.Frontiers in cellular and infection microbiology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Decay of the HIV reservoir is slowed over time in part by expansion of the pool of HIV-infected cells. This expansion reflects homeostatic proliferation of infected cells by interleukin-7 (IL-7) or antigenic stimulation, as well as new rounds of infection of susceptible target cells. As novel therapies are being developed to accelerate the decay of the latent HIV reservoir, it will be important to identify interventions that prevent expansion and/or repopulation of the latent HIV reservoir. Our previous studies showed that HIV protease cleaves the host protein procaspase 8 to generate Casp8p41, which can bind and activate Bak to induce apoptosis of infected cells. In circumstances where expression of the anti-apoptotic protein BCL2 is high, Casp8p41 instead binds BCL2, and cell death does not occur. This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell. Here we assess whether the events that maintain the HIV reservoir are also antagonized by venetoclax. Using the J-Lat 10.6 model of persistent infection, we demonstrate that proliferation and HIV expression are countered by the use of venetoclax, which causes preferential killing of the HIV-expressing cells. Similarly, during new rounds of infection of primary CD4 T cells, venetoclax causes selective killing of HIV-infected cells, resulting in decreased numbers of HIV DNA-containing 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.