ArticleJournal of virology2013
Myeloblastic cell lines mimic some but not all aspects of human cytomegalovirus experimental latency defined in primary CD34+ cell populations.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 47 citations in OpenAlex.
- Human Cytomegalovirus UL4 is Required for Viral Reactivation via Cellular Reprogramming in Latently Infected CD34+ Progenitor Cells and Humanized Mice.bioRxiv : the preprint server for biology · 2026Article
- Cytomegalovirus latency-the sum of subtleties.Journal of virology · 2025Review
- Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.Tumour virus research · 2025Review
- Inhibition of MAPK signaling suppresses cytomegalovirus reactivation in CD34Antiviral research · 2025Article
- Repurposing an endogenous degradation domain for antibody-mediated disposal of cell-surface proteins.EMBO reports · 2024Article
- NFκB and Cyclic AMP Response Element Sites Mediate the Valproic Acid and UL138 Responsiveness of the Human Cytomegalovirus Major Immediate Early Enhancer and Promoter.Journal of virology · 2023Article
- Hematopoietic-Mesenchymal Signals Regulate the Properties of Mesenchymal Stem Cells.International journal of molecular sciences · 2022Article
- Human cytomegalovirus lytic infection inhibits replication-dependent histone synthesis and requires stem loop binding protein function.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- Article
- Epigenetic reprogramming of host and viral genes by Human Cytomegalovirus infection in Kasumi-3 myeloid progenitor cells at early times post-infection.Journal of virology · 2021Article
- Bromodomain proteins regulate human cytomegalovirus latency and reactivation allowing epigenetic therapeutic intervention.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- CD34Journal of virology · 2021Article
- Human Cytomegalovirus Decreases Major Histocompatibility Complex Class II by Regulating Class II Transactivator Transcript Levels in a Myeloid Cell Line.Journal of virology · 2020Article
- Evidence for Tethering of Human Cytomegalovirus Genomes to Host Chromosomes.Frontiers in cellular and infection microbiology · 2020Article
- Expanding the Known Functional Repertoire of the Human Cytomegalovirus pp71 Protein.Frontiers in cellular and infection microbiology · 2020Review
- Cell Line Models for Human Cytomegalovirus Latency Faithfully Mimic Viral Entry by Macropinocytosis and Endocytosis.Journal of virology · 2019Article
- The Golgi sorting motifs of human cytomegalovirus UL138 are not required for latency maintenance.Virus research · 2019Article
- Alternative promoters drive human cytomegalovirus reactivation from latency.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human Cytomegalovirus Enters the Primary CD34Journal of virology · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human cytomegalovirus (HCMV) is a significant human pathogen that achieves lifelong persistence by establishing latent infections in undifferentiated cells of the myeloid lineage, such as CD34(+) hematopoietic progenitor cells. When latency is established, viral lytic gene expression is silenced in part by a cellular intrinsic defense consisting of Daxx and histone deacetylases (HDACs) because pp71, the tegument transactivator that travels to the nucleus and inactivates this defense at the start of a lytic infection in differentiated cells, remains in the cytoplasm. Because the current in vitro and ex vivo latency models have physiological and practical limitations, we evaluated two CD34(+) myeloblastic cell lines, KG-1 and Kasumi-3, for their ability to establish, maintain, and reactivate HCMV experimental latent infections. Tegument protein pp71 was cytoplasmic, and immediate-early (IE) genes were silenced as in primary CD34(+) cells. However, in contrast to what occurs in primary CD34(+) cells ex vivo or in NT2 and THP-1 in vitro model systems, viral IE gene expression from the laboratory-adapted AD169 genome was not induced in the presence of HDAC inhibitors in either KG-1 or Kasumi-3 cells. Furthermore, while the clinical strain FIX was able to reactivate from Kasumi-3 cells, AD169 was not, and neither strain reactivated from KG-1 cells. Thus, KG-1 and Kasumi-3 experimental latent infections differ in important parameters from those in primary CD34(+) cell populations. Aspects of latency illuminated through the use of these myeloblastoid cell lines should not be considered independently but integrated with results obtained in primary cell systems when paradigms for HCMV latency are proposed.
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