ArticleJournal of virology2002
Infection of cells with human cytomegalovirus during S phase results in a blockade to immediate-early gene expression that can be overcome by inhibition of the proteasome.
Article in Journal of virology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 79 citations in OpenAlex.
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- Essentiality and dynamic expression of the human tRNA pool during viral infection.Molecular systems biology · 2026Article
- Viral entry shapes HCMV latency establishment.Nature communications · 2025Article
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- Sirtuin 2 promotes human cytomegalovirus replication by regulating cell cycle progression.mSystems · 2023Article
- Human cytomegalovirus RNA2.7 inhibits RNA polymerase II (Pol II) Serine-2 phosphorylation by reducing the interaction between Pol II and phosphorylated cyclin-dependent kinase 9 (pCDK9).Virologica Sinica · 2022Article
- Virus-host protein interactions as footprints of human cytomegalovirus replication.Current opinion in virology · 2022Review
- The aryl hydrocarbon receptor facilitates the human cytomegalovirus-mediated G1/S block to cell cycle progression.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cytomegalovirus in Haematological Tumours.Frontiers in immunology · 2021Review
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- The constitutive activity of the viral-encoded G protein-coupled receptor US28 supports a complex signalling network contributing to cancer development.Biochemical Society transactions · 2020Review
- Human cytomegalovirus glycoprotein B variants affect viral entry, cell fusion, and genome stability.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- A Noncanonical Function of Polycomb Repressive Complexes Promotes Human Cytomegalovirus Lytic DNA Replication and Serves as a Novel Cellular Target for Antiviral Intervention.Journal of virology · 2019Article
- Activation of E2F-dependent transcription by the mouse cytomegalovirus M117 protein affects the viral host range.PLoS pathogens · 2018Article
- Human cytomegalovirus and Herpes Simplex type I virus can engage RNA polymerase I for transcription of immediate early genes.Oncotarget · 2017Article
- The host ubiquitin-dependent segregase VCP/p97 is required for the onset of human cytomegalovirus replication.PLoS pathogens · 2017Article
- Synthetic lethal mutations in the cyclin A interface of human cytomegalovirus.PLoS pathogens · 2017Article
- Expression of Oncogenic Alleles Induces Multiple Blocks to Human Cytomegalovirus Infection.Journal of virology · 2016Article
- Human cytomegalovirus riding the cell cycle.Medical microbiology and immunology · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cells infected with human cytomegalovirus (HCMV) after commencing DNA replication do not initiate viral immediate-early (IE) gene expression and divide before arresting. To determine the nature of this blockade, we examined cells that were infected 24 h after release from G(0) using immunofluorescence, laser scanning cytometry, and fluorescence-activated cell sorting (FACS) analysis. Approximately 40 to 50% of the cells had 2N DNA content, became IE(+) in the first 12 h, and arrested. Most but not all of the cells with >2N DNA content did not express IE antigens until after mitosis. To define the small population of IE(+) cells that gradually accumulated within the S and G(2)/M compartments, cells were pulsed with bromodeoxyuridine (BrdU) just prior to S-phase infection and analyzed at 12 h postinfection for IE gene expression, BrdU positivity, and cell cycle position. Most of the BrdU(+) cells were IE(-) and had progressed into G(2)/M or back to G(1). The majority of the IE(+) cells in S and G(2)/M were BrdU(-). Only a few cells were IE(+) BrdU(+), and they resided in G(2)/M. Multipoint BrdU pulse-labeling revealed that, compared to cells actively synthesizing DNA at the beginning of the infection, a greater percentage of the cells that initiated DNA replication 4 h later could express IE antigens and proceed into S. Synchronization of the cells with aphidicolin also indicated that the blockade to the activation of IE gene expression was established in cells soon after initiation of DNA replication. It appears that a short-lived protein in S-phase cells may be required for IE gene expression, as it is partially restored by treatment with the proteasome inhibitor MG132.
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