ArticleJournal of virology1999
Truncation of the C-terminal acidic transcriptional activation domain of herpes simplex virus VP16 renders expression of the immediate-early genes almost entirely dependent on ICP0.
Article in Journal of virology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 53 citations in OpenAlex.
- The 4EHP-mediated translational repression of cGAS impedes the host immune response against DNA viruses.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Sp1 facilitates continued HSV-1 gene expression in the absence of key viral transactivators.mBio · 2024Article
- The precise function of alphaherpesvirus tegument proteins and their interactions during the viral life cycle.Frontiers in microbiology · 2024Review
- Carnitine palmitoyl-transferase 1A is potentially involved in bovine herpesvirus 1 productive infection.Veterinary microbiology · 2024Article
- Host factors associated with either VP16 or VP16-induced complex differentially affect HSV-1 lytic infection.Reviews in medical virology · 2022Review
- Multi-phenotype analysis for enhanced classification of 11 herpes simplex virus 1 strains.The Journal of general virology · 2022Article
- An Essential Viral Transcription Activator Modulates Chromatin Dynamics.PLoS pathogens · 2016Article
- Article
- Oncolytic virotherapy using herpes simplex virus: how far have we come?Oncolytic virotherapy · 2015Review
- Permissiveness of human cancer cells to oncolytic bovine herpesvirus 1 is mediated in part by KRAS activity.Journal of virology · 2014Article
- Review
- The differential mobilization of histones H3.1 and H3.3 by herpes simplex virus 1 relates histone dynamics to the assembly of viral chromatin.PLoS pathogens · 2013Article
- Core histones H2B and H4 are mobilized during infection with herpes simplex virus 1.Journal of virology · 2011Article
- Adaptive antiviral immunity is a determinant of the therapeutic success of oncolytic virotherapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- Herpes simplex virus VP16, but not ICP0, is required to reduce histone occupancy and enhance histone acetylation on viral genomes in U2OS osteosarcoma cells.Journal of virology · 2010Article
- Cell fusion-induced activation of interferon-stimulated genes is not required for restriction of a herpes simplex virus VP16/ICP0 mutant in heterokarya formed between permissive and restrictive cells.Journal of virology · 2009Article
- PML has a predictive role in tumor cell permissiveness to interferon-sensitive oncolytic viruses.Gene therapy · 2009Article
- Epigenetic modulation of gene expression from quiescent herpes simplex virus genomes.Journal of virology · 2009Article
- Analysis of the functions of herpes simplex virus type 1 regulatory protein ICP0 that are critical for lytic infection and derepression of quiescent viral genomes.Journal of virology · 2009Article
- De novo synthesis of VP16 coordinates the exit from HSV latency in vivo.PLoS pathogens · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The herpes simplex virus (HSV) proteins VP16 and ICP0 play key roles in stimulating the onset of the viral lytic cycle. We sought to explore the regulatory links between these proteins by studying the phenotypes of viral mutants in which the activation functions of both were simultaneously inactivated. This analysis unexpectedly revealed that truncation of the C-terminal transcriptional activation domain of VP16 (allele V422) in an ICP0-deficient background almost completely eliminated immediate-early gene expression and virus replication in Vero and HEL cells. The doubly mutant viral genome persisted in a quiescent state for at least 10 days in HEL cells infected at high multiplicity and could be reactivated by superinfection with wild-type HSV. In contrast, the in1814 VP16 mutation produced a markedly less severe phenotype in the same ICP0-deficient background. These data demonstrate that expression of the immediate-early genes requires ICP0 when the C-terminal activation domain of VP16 is deleted and raise the possibility that the in1814 form of VP16 retains a residual ability to stimulate gene expression during virus infection.
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.