Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Inhibitors Of Virion Release01:25

Inhibitors Of Virion Release

Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Circular RNA dynamics in breast-to-brain metastatic cascade.

BMC biology·2026
Same author

IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.

Nature communications·2026
Same author

Publisher Correction: Tumor transcriptional state predicts survival in immune-checkpoint-blockade-treated glioblastoma.

Nature cancer·2026
Same author

Tumor transcriptional state predicts survival in immune-checkpoint-blockade-treated glioblastoma.

Nature cancer·2026
Same author

A standardized single-tube 17-color spectral flow cytometry workflow for integrated immunophenotyping of human PBMCs and mixed co-culture systems.

Frontiers in immunology·2026
Same author

Treatment Effect Reanalysis of the Randomized Individual Screening Trial of Innovative Glioblastoma Therapy in Newly Diagnosed Glioblastoma With External Control Data.

Journal of clinical oncology : official journal of the American Society of Clinical Oncology·2026

Related Experiment Video

Updated: Jun 25, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy
06:40

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Published on: November 4, 2018

ICP0 inhibits the decrease of HSV amplicon-mediated transgene expression.

Masataka Suzuki1, Kazue Kasai, Akihiro Ohtsuki

  • 1Dardinger Laboratory for Neuro-oncology and Neurosciences, Department of Neurological Surgery, James Comprehensive Cancer Center and The Ohio State University Medical Center, Columbus, Ohio 43210, USA.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|February 19, 2009
PubMed
Summary
This summary is machine-generated.

Restoring herpes simplex virus (HSV) infected cell protein 0 (ICP0) in amplicon vectors enhances transgene expression. This approach overcomes host responses that limit gene therapy efficacy, showing promise for in vivo applications.

More Related Videos

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
11:56

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1

Published on: August 24, 2015

Related Experiment Videos

Last Updated: Jun 25, 2026

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy
06:40

Temporal Analysis of the Nuclear-to-cytoplasmic Translocation of a Herpes Simplex Virus 1 Protein by Immunofluorescent Confocal Microscopy

Published on: November 4, 2018

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1
11:56

Ex Vivo Infection of Murine Epidermis with Herpes Simplex Virus Type 1

Published on: August 24, 2015

Area of Science:

  • Gene therapy
  • Virology
  • Molecular biology

Background:

  • Herpes simplex virus (HSV) amplicon vectors are used for gene delivery.
  • Host immune responses can limit transgene expression from these vectors.
  • Silencing of transgenes is a major hurdle in gene therapy.

Purpose of the Study:

  • To investigate if restoring HSV infected cell protein 0 (ICP0) expression in amplicon vectors can overcome host-mediated transgene silencing.
  • To evaluate the impact of ICP0 on vector-induced host responses and transgene expression kinetics.

Main Methods:

  • Construction of an ICP0-expressing HSV amplicon vector (ICP0+ amplicon).
  • Assessment of ICP0 expression, host responses (interferon), cell kinetics, and apoptosis.
  • Chromatin immunoprecipitation (ChIP) PCR to analyze histone deacetylase 1 (HDAC1) association with amplicon DNA.
  • In vivo studies in mice to compare transgene expression from ICP0+ and conventional amplicons in the liver.

Main Results:

  • ICP0 expression was transient and did not significantly affect host responses or cell viability at a multiplicity of infection (MOI) of 1.
  • ICP0+ amplicon DNA showed reduced association with HDAC1 compared to conventional amplicons.
  • Mice treated with ICP0+ amplicons demonstrated significantly higher and more sustained transgene expression in the liver.

Conclusions:

  • Restoration of ICP0 expression in HSV amplicon vectors can effectively reduce transgene silencing.
  • ICP0 enhances transgene expression likely through increased transcriptional or post-transcriptional activity.
  • ICP0-expressing HSV amplicon vectors represent a promising strategy for improving gene therapy efficacy in vitro and in vivo.