ArticleRetrovirology2016
The interferon-induced antiviral protein PML (TRIM19) promotes the restriction and transcriptional silencing of lentiviruses in a context-specific, isoform-specific fashion.
Article in Retrovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions.Frontiers in immunology · 2026Review
- A Canadian Survey of Research on HIV-1 Latency-Where Are We Now and Where Are We Heading?Viruses · 2024Review
- PML Alternative Splice Products Differentially Regulate HAdV Productive Infection.Microbiology spectrum · 2022Article
- Interplay between RNA Viruses and Promyelocytic Leukemia Nuclear Bodies.Veterinary sciences · 2021Review
- Regulation of Tripartite Motif-Containing Proteins on Immune Response and Viral Evasion.Frontiers in microbiology · 2021Review
- Editing of the TRIM5 Gene Decreases the Permissiveness of Human T Lymphocytic Cells to HIV-1.Viruses · 2020Article
- Vertical transmission of hepatitis E virus in pregnant rhesus macaques.Scientific reports · 2020Article
- The Restrictome of Flaviviruses.Virologica Sinica · 2020Review
- Interferon-γ signaling in human iPSC-derived neurons recapitulates neurodevelopmental disorder phenotypes.Science advances · 2020Article
- MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling.Nature communications · 2020Article
- To TRIM or not to TRIM: the balance of host-virus interactions mediated by the ubiquitin system.The Journal of general virology · 2019Article
- Tripartite motif proteins: an emerging antiviral protein family.Future virology · 2019Article
- TRIM15 Exerts Anti-Tumor Effects Through Suppressing Cancer Cell Invasion in Gastric Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- HIV-1 capsids from B27/B57+ elite controllers escape Mx2 but are targeted by TRIM5α, leading to the induction of an antiviral state.PLoS pathogens · 2018Article
- Oncogenic TRIM31 confers gemcitabine resistance in pancreatic cancer via activating the NF-κB signaling pathway.Theranostics · 2018Article
- Intracellular Antiviral Immunity.Advances in virus research · 2018Review
- Editing of the human TRIM5 gene to introduce mutations with the potential to inhibit HIV-1.PloS one · 2018Article
- The TRIMendous Role of TRIMs in Virus-Host Interactions.Vaccines · 2017Review
- Tripartite Motif-Containing Protein 22 Interacts with Class II Transactivator and Orchestrates Its Recruitment in Nuclear Bodies Containing TRIM19/PML and Cyclin T1.Frontiers in immunology · 2017Article
- Tripartite Motif 22 and Class II Transactivator Restriction Factors: Unveiling Their Concerted Action against Retroviruses.Frontiers in immunology · 2017Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe promyelocytic leukemia (PML) protein, a type I interferon (IFN-I)-induced gene product and a member of the tripartite motif (TRIM) family, modulates the transcriptional activity of viruses belonging to various families. Whether PML has an impact on the replication of HIV-1 has not been fully addressed, but recent studies point to its possible involvement in the restriction of HIV-1 in human cells and in the maintenance of transcriptional latency in human cell lines in which HIV-1 is constitutively repressed. We investigated further the restriction of HIV-1 and a related lentivirus, SIVmac, by PML in murine cells and in a lymphocytic human cell line. In particular, we studied the relevance of PML to IFN-I-mediated inhibition and the role of individual human isoforms.
resultsWe demonstrate that both human PML (hPML) and murine PML (mPML) inhibit the early post-entry stages of the replication of HIV-1 and a related lentivirus, SIVmac. In addition, HIV-1 was transcriptionally silenced by mPML and by hPML isoforms I, II, IV and VI in MEFs. This PML-mediated transcriptional repression was attenuated in presence of the histone deacetylase inhibitor SAHA. In contrast, depletion of PML had no effect on HIV-1 gene expression in a human T cell line. PML was found to contribute to the inhibition of HIV-1 by IFN-I. Specifically, IFN-α and IFN-β treatments of MEFs enhanced the PML-dependent inhibition of HIV-1 early replication stages.
conclusionsWe show that PML can inhibit HIV-1 and other lentiviruses as part of the IFN-I-mediated response. The restriction takes place at two distinct steps, i.e. reverse transcription and transcription, and in an isoform-specific, cellular context-specific fashion. Our results support a model in which PML activates innate immune antilentiviral effectors. These data are relevant to the development of latency reversal-inducing pharmacological agents, since PML was previously proposed as a pharmacological target for such inhibitors. This study also has implications for the development of murine models of HIV-1.
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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.