ArticleJournal of virology1997
Repression of host RNA polymerase II transcription by herpes simplex virus type 1.
Article in Journal of virology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed.
- 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
- Herpesviruses: overview of systematics, genomic complexity and life cycle.Virology journal · 2025Review
- HSV-1 infection induces a downstream shift of the +1 nucleosome.Journal of virology · 2025Article
- Herpes simplex virus 1 inhibits phosphorylation of RNA polymerase II CTD serine-7.Journal of virology · 2024Article
- Review
- Several Alphaherpesviruses Interact Similarly with the NF-κB Pathway and Suppress NF-κB-Dependent Gene Expression.Microbiology spectrum · 2023Article
- Cellular state landscape and herpes simplex virus type 1 infection progression are connected.Nature communications · 2023Article
- HSV-1 Infection Induces a Downstream Shift of Promoter-Proximal Pausing for Host Genes.Journal of virology · 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
- ICP22 of Herpes Simplex Virus 1 Decreases RNA Polymerase Processivity.Journal of virology · 2022Article
- HSV-1 and influenza infection induce linear and circular splicing of the long NEAT1 isoform.PloS one · 2022Article
- The Herpes Simplex Virus 1 Protein ICP4 Acts as both an Activator and a Repressor of Host Genome Transcription during Infection.Molecular and cellular biology · 2021Article
- A Review of the Multipronged Attack of Herpes Simplex Virus 1 on the Host Transcriptional Machinery.Viruses · 2021Review
- Widespread remodeling of the mProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Feline Calicivirus Proteinase-Polymerase Protein Degrades mRNAs To Inhibit Host Gene Expression.Journal of virology · 2021Article
- Dissecting Herpes Simplex Virus 1-Induced Host Shutoff at the RNA Level.Journal of virology · 2021Article
- "Non-Essential" Proteins of HSV-1 with Essential Roles In Vivo: A Comprehensive Review.Viruses · 2020Review
- RNA decay during gammaherpesvirus infection reduces RNA polymerase II occupancy of host promoters but spares viral promoters.PLoS pathogens · 2020Article
- HSV-1 triggers paracrine fibroblast growth factor response from cortical brain cells via immediate-early protein ICP0.Journal of neuroinflammation · 2019Article
10 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
3 authors.
Funding
Abstract
Lytic infection of mammalian cells with herpes simplex virus type 1 (HSV-1) results in rapid repression of host gene expression and selective activation of the viral genome. This transformation in gene expression is thought to involve repression of host transcription and diversion of the host RNA polymerase (RNAP II) transcription machinery to the viral genome. However, the extent of virus-induced host transcription repression and the mechanisms responsible for these major shifts in transcription specificities have not been examined. To determine how HSV-1 accomplishes repression of host RNAP II transcription, we assayed transcription patterns on several cellular genes in cells infected with mutant and wild-type HSV-1. Our results suggest that HSV-1 represses RNAP II transcription on most cellular genes. However, each cellular gene we examined responds differently to the transcription repressive effects of virus infection, both quantitatively and with respect to the involvement of viral gene products. Virus-induced shutoff of host RNAP II transcription requires expression of multiple immediate-early genes. In contrast, expression of delayed-early and late genes and viral DNA replication appear to contribute little to repression of host cell RNAP II transcription. Modification of RNAP II to the intermediately phosphorylated (II(I)) form appears unlinked to virus-induced repression of host cell transcription. However, full repression of host transcription is correlated with depletion of the hyperphosphorylated (IIO) form of RNAP II.
Indexed as
Identifiers
What OpenQuestion holds
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.