ArticleJournal of virology2003
Recruitment of herpes simplex virus type 1 transcriptional regulatory protein ICP4 into foci juxtaposed to ND10 in live, infected cells.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 109 citations in OpenAlex.
- Nucleus softens during herpesvirus infection.PLoS pathogens · 2026Article
- Liquid-Liquid Phase Separation: Mechanisms, Roles, and Implications in Cellular Function and Disease.FASEB bioAdvances · 2025Review
- Chromatin Regulation of HSV Gene Transcription.Viruses · 2025Review
- Daxx mediated histone H3.3 deposition on HSV-1 DNA restricts genome decompaction and the progression of immediate-early transcription.PLoS pathogens · 2025Article
- Lineage memory shapes viral resistance barriers in human skin.bioRxiv : the preprint server for biology · 2025Article
- The S-Phase Arrest of Host Cells Caused by an Alpha-Herpesvirus Genome Replication Facilitates Viral Recruitment of RNA Polymerase II to Transcribe Viral Genes.Cell proliferation · 2025Article
- HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal.The Journal of clinical investigation · 2023Article
- Two-Color CRISPR Imaging Reveals Dynamics of Herpes Simplex Virus 1 Replication Compartments and Virus-Host Interactions.Journal of virology · 2022Article
- Article
- Herpes Simplex Virus 1 Can Bypass Impaired Epidermal Barriers uponJournal of virology · 2022Article
- Article
- When liquid-liquid phase separation meets viral infections.Frontiers in immunology · 2022Review
- Parallel G-quadruplexes recruit the HSV-1 transcription factor ICP4 to promote viral transcription in herpes virus-infected human cells.Communications biology · 2021Article
- The HSV-1 Transcription Factor ICP4 Confers Liquid-Like Properties to Viral Replication Compartments.International journal of molecular sciences · 2021Article
- Article
- Review
- The HSV-1 ICP4 Transcriptional Auto-Repression Circuit Functions as a Transcriptional "Accelerator" Circuit.Frontiers in cellular and infection microbiology · 2020Article
- Article
- Quantitative Microscopy Reveals Stepwise Alteration of Chromatin Structure during Herpesvirus Infection.Viruses · 2019Article
- Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At the early stages of herpes simplex virus type 1 (HSV-1) infection, parental viral genomes have a tendency to become juxtaposed to cellular nuclear structures known as PML (promyelocytic leukemia) nuclear bodies or ND10, while the immediate-early (IE) protein ICP0 precisely colocalizes with these structures. Previous indirect-immunofluorescence studies observed that the HSV-1 transcriptional regulator ICP4 has a mainly diffuse nuclear distribution early in infection and is later recruited into viral replication compartments. We have constructed HSV-1 variants expressing ICP4 and ICP0 linked to ECFP and EYFP, respectively, both singly and in combination. Coupled with an efficient method of expressing autofluorescent PML in ND10, we have studied the dynamics of ICP0, ICP4, and ND10 in live, infected cells. The greater sensitivity and lower background signals in live cells revealed that early in infection, ICP4 forms discrete foci, some of which are juxtaposed to ND10, while ICP0 was found to colocalize precisely with PML. As expected from these results, using a double-labeled virus, we observed that foci of ICP0 and ICP4 were also juxtaposed but not colocalized early in infection. Some of the ICP4 foci must have contained parental viral genomes, because they developed into replication compartments. We propose that a proportion of the ND10-associated ICP4 foci represent ICP4 molecules being recruited onto parental viral genomes, a process likely to be a critical step early in lytic infection. These results may be analogous to the localization of IE1 and IE2 during human cytomegalovirus infection, suggesting a principle common to the alpha- and betaherpesviruses.
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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.