ArticleJournal of virology2000
Herpes simplex virus type 1 ICP0 protein does not accumulate in the nucleus of primary neurons in culture.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Next-generation replication-defective HSV vectors for delivery of large DNA payloads.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Evaluation of parameters for efficient purification and long-term storage of herpes simplex virus-based vectors.Molecular therapy. Methods & clinical development · 2022Article
- The Cyclin-Dependent Kinase 5 Inhibitor Peptide Inhibits Herpes Simplex Virus Type 1 Replication.Scientific reports · 2019Article
- Herpes Simplex Virus Vectors for Gene Transfer to the Central Nervous System.Diseases (Basel, Switzerland) · 2018Review
- Deletion of the Virion Host Shut-off Gene Enhances Neuronal-Selective Transgene Expression from an HSV Vector Lacking Functional IE Genes.Molecular therapy. Methods & clinical development · 2017Article
- Latency Entry of Herpes Simplex Virus 1 Is Determined by the Interaction of Its Genome with the Nuclear Environment.PLoS pathogens · 2016Article
- Herpes Simplex Virus 1 Infection of Tree Shrews Differs from That of Mice in the Severity of Acute Infection and Viral Transcription in the Peripheral Nervous System.Journal of virology · 2016Article
- Herpes simplex viral-vector design for efficient transduction of nonneuronal cells without cytotoxicity.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Novel mutations in gB and gH circumvent the requirement for known gD Receptors in herpes simplex virus 1 entry and cell-to-cell spread.Journal of virology · 2013Article
- Herpes simplex virus requires poly(ADP-ribose) polymerase activity for efficient replication and induces extracellular signal-related kinase-dependent phosphorylation and ICP0-dependent nuclear localization of tankyrase 1.Journal of virology · 2012Article
- Mechanism of HSV infection through soluble adapter-mediated virus bridging to the EGF receptor.Virology · 2011Article
- Bispecific adapter-mediated retargeting of a receptor-restricted HSV-1 vector to CEA-bearing tumor cells.Molecular therapy : the journal of the American Society of Gene Therapy · 2011Article
- A herpes simplex virus vector system for expression of complex cellular cDNA libraries.Journal of virology · 2010Article
- Article
- Towards an understanding of the herpes simplex virus type 1 latency-reactivation cycle.Interdisciplinary perspectives on infectious diseases · 2010Article
- Effects of transgene-mediated endomorphin-2 in inflammatory pain.European journal of pain (London, England) · 2009Article
- Herpes simplex virus vector-mediated delivery of neurturin rescues erectile dysfunction of cavernous nerve injury.Gene therapy · 2009Article
- Identification and characterization of a new E3 ubiquitin ligase in white spot syndrome virus involved in virus latency.Virology journal · 2008Article
- Relaxed repression of herpes simplex virus type 1 genomes in Murine trigeminal neurons.Journal of virology · 2007Article
- Equine herpesvirus 1 enters cells by two different pathways, and infection requires the activation of the cellular kinase ROCK1.Journal of virology · 2007Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infected-cell protein 0 (ICP0), the product of the herpes simplex virus (HSV) immediate-early (IE) alpha0 gene, is a promiscuous transactivator of viral early (E) and late (L) gene expression. HSV mutants lacking ICP0 function are severely deficient in viral growth and protein synthesis, particularly at low multiplicities of infection. Early in the infectious process in vitro, ICP0 protein accumulates in distinct domains within the nucleus to form characteristic structures active in the transcription of viral genes. However, following infection of primary trigeminal ganglion cells in vitro with a recombinant HSV mutant that expresses only ICP0, we observed that ICP0 protein accumulated in the characteristic intranuclear distribution only in the nuclei of Schwann cells; neurons in the culture did not accumulate ICP0 despite expression of ICP0 RNA in those cells. The same phenomenon was observed in PC12 cells differentiated to assume a neuronal phenotype. In primary neurons in culture, the amount of ICP0 protein could be increased by pharmacologic inhibition of calcium-activated protease (calpain) activity or by inhibition of protein phosphatase 2B (calcineurin). The failure of ICP0 protein to accumulate in the nucleus of neurons suggests that one mechanism which may impair efficient replication of the virus in neurons, and thus favor the establishment of viral latency in those cells, may be found in the cell-specific processing of that IE gene product.
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