ArticleRetrovirology2015
Apoptosis-induced activation of HIV-1 in latently infected cell lines.
Article in Retrovirology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Inhibition of CDK12/CDK13-CYCLIN K rewires P-TEFb signaling to reverse HIV-1 latency and modulate cellular gene expression.EMBO molecular medicine · 2026Article
- HIV associated cell death: Peptide-induced apoptosis restricts viral transmission.Frontiers in immunology · 2023Article
- Host Cell Redox Alterations Promote Latent HIV-1 Reactivation through Atypical Transcription Factor Cooperativity.Viruses · 2022Article
- T cell stimulation remodels the latently HIV-1 infected cell population by differential activation of proviral chromatin.PLoS pathogens · 2022Article
- U1 and OM10.1. Myeloid Cell Lines as Surrogate Models of Reversible Proviral Latency.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Hydrogen sulfide blocks HIV rebound by maintaining mitochondrial bioenergetics and redox homeostasis.eLife · 2021Article
- Antioxidant nanozyme counteracts HIV-1 by modulating intracellular redox potential.EMBO molecular medicine · 2021Article
- Identification of celastrol as a novel HIV-1 latency reversal agent by an image-based screen.PloS one · 2021Article
- Alterations of redox and iron metabolism accompany the development of HIV latency.The EMBO journal · 2020Article
- Novel pathways of HIV latency reactivation revealed by integrated analysis of transcriptome and target profile of bryostatin.Scientific reports · 2020Article
- Chromatin maturation of the HIV-1 provirus in primary resting CD4+ T cells.PLoS pathogens · 2020Article
- Cat and Mouse: HIV Transcription in Latency, Immune Evasion and Cure/Remission Strategies.Viruses · 2019Review
- Serum deprivation/starvation leads to reactivation of HIV-1 in latently infected monocytes via activating ERK/JNK pathway.Scientific reports · 2018Article
- HIV-1 replication in CD4Virology · 2018Article
- Cell Death Is Counteracted by Mitophagy in HIV-Productively Infected Astrocytes but Is Promoted by Inflammasome Activation Among Non-productively Infected Cells.Frontiers in immunology · 2018Article
- Combination of a Latency-Reversing Agent With a Smac Mimetic Minimizes Secondary HIV-1 InfectionFrontiers in microbiology · 2018Article
- The nature and nurture of cell heterogeneity: accounting for macrophage gene-environment interactions with single-cell RNA-Seq.BMC genomics · 2017Article
- Absence of autophagy promotes apoptosis by modulating the ROS-dependent RLR signaling pathway in classical swine fever virus-infected cells.Autophagy · 2016Article
- Highly activated p53 contributes to selectively increased apoptosis of latently HIV-1 infected cells upon treatment of anticancer drugs.Virology journal · 2016Article
- Dual targeting of the thioredoxin and glutathione systems in cancer and HIV.The Journal of clinical investigation · 2016Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDespite much work, safe and effective approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1 remain an elusive goal. Patients infected with HIV-1 treated with cytotoxic agents or bone marrow transplantation can experience decreases in the reservoir of HIV-1 latently infected cells. Other viruses capable of long-term latency, such as herpesviruses, can sense host cell apoptosis and respond by initiating replication. These observations suggest that other viruses capable of long-term latency, like HIV-1, might also sense when its host cell is about to undergo apoptosis and respond by initiating replication.
resultsPro-monocytic (U1) and lymphoid (ACH-2) HIV-1 persistently infected cell lines were treated with cytotoxic drugs - doxorubicin, etoposide, fludarabine phosphate, or vincristine - and activation of latent HIV-1 was evaluated using assays for HIV-1 RNA and p24 production. Both cell lines showed dose-dependent increases in apoptosis and associated HIV-1 activation following exposure to the cytotoxic agents. Pretreatment of the cells with the pan-caspase inhibitor Z-VAD-FMK prior to exposure to the cytotoxic agents inhibited apoptosis and viral activation. Direct exposure of the latently infected cell lines to activated caspases also induced viral replication. HIV-1 virions produced in association with host cell apoptosis were infectious.
conclusionsThe results indicate that latent HIV-1 can sense when its host cell is undergoing apoptosis and responds by completing its replication cycle. The results may help explain why patients treated with cytotoxic regimens for bone marrow transplantation showed reductions in the reservoir of latently infected cells. The results also suggest that the mechanisms that HIV-1 uses to sense and respond to host cell apoptosis signals may represent helpful new targets for approaches to attack and deplete the long-lived reservoir of cells latently infected with HIV-1.
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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.