ArticleeLife2015
Release of human cytomegalovirus from latency by a KAP1/TRIM28 phosphorylation switch.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 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
96 citing papers in PubMed, 127 citations in OpenAlex.
- Subclinical Reactivation of Cytomegalovirus Drives CD4+CD28null T-Cell Expansion and Impaired Immune Response to Pneumococcal Vaccination in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis.The Journal of infectious diseases · 2019Trial
- Mechanisms and Determinants of CMV Reactivation in Kidney Transplantation.International journal of molecular sciences · 2026Review
- Sensing the storm: how inflammatory signalling drives reactivation of the human cytomegalovirus major immediate-early promoter.The Journal of general virology · 2026Review
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- The role of KRAB zinc-finger proteins in expanding the domestication potential of transposable elements.Nature genetics · 2026Review
- Article
- Viral entry shapes HCMV latency establishment.Nature communications · 2025Article
- Lytic or Latent Phase in Human Cytomegalovirus Infection: An Epigenetic Trigger.International journal of molecular sciences · 2025Review
- Cytoplasmic translocation of tripartite motif-containing 28 is critical for PRRSV-induced autophagy through promoting Vps34-Beclin1 complex formation.Journal of virology · 2025Article
- TRIM28 is a target for paramyxovirus V proteins.PLoS pathogens · 2025Article
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025Review
- Insights into the protein domains of C-VI TRIM subfamily in viral infection.Frontiers in cellular and infection microbiology · 2025Review
- Human cytomegalovirus infection induces L1 expression through UL38-dependent mTOR-KAP1 pathway.PloS one · 2025Article
- The HUSH epigenetic repressor complex silences PML nuclear body-associated HSV-1 quiescent genomes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- KAP1/TRIM28 - antiviral and proviral protagonist of herpesvirus biology.Trends in microbiology · 2024Article
- An epigenetic human cytomegalovirus infection score predicts viremia risk in seropositive lung transplant recipients.Epigenetics · 2024Article
- XAF1 antagonizes TRIM28 activity through the assembly of a ZNF313-mediated destruction complex to suppress tumor malignancy.Molecular biomedicine · 2024Article
- Review
- Human cytomegalovirus harnesses host L1 retrotransposon for efficient replication.Nature communications · 2024Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Human cytomegalovirus (HCMV) is a highly prevalent pathogen that induces life-long infections notably through the establishment of latency in hematopoietic stem cells (HSC). Bouts of reactivation are normally controlled by the immune system, but can be fatal in immuno-compromised individuals such as organ transplant recipients. Here, we reveal that HCMV latency in human CD34(+) HSC reflects the recruitment on the viral genome of KAP1, a master co-repressor, together with HP1 and the SETDB1 histone methyltransferase, which results in transcriptional silencing. During lytic infection, KAP1 is still associated with the viral genome, but its heterochromatin-inducing activity is suppressed by mTOR-mediated phosphorylation. Correspondingly, HCMV can be forced out of latency by KAP1 knockdown or pharmacological induction of KAP1 phosphorylation, and this process can be potentiated by activating NFkB with TNF-α. These results suggest new approaches both to curtail CMV infection and to purge the virus from organ transplants.
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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.