Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Inhibitors of Viral Protein Synthesis

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

Author Correction: ICP4-induced miR-101 attenuates HSV-1 replication.

Scientific reports·2021

Same author

Localized Surface Plasmon Resonance Induced Band Gap Regulation Governing the Excellent Photocatalytic Performance of Ag/g-C₃N₄ Heterostructure.

Journal of nanoscience and nanotechnology·2019

Same author

Immunomodulatory Biscembranoids and Assignment of Their Relative and Absolute Configurations: Data Set Modulation in the Density Functional Theory/Nuclear Magnetic Resonance Approach.

Journal of natural products·2019

Same author

TNF-α-induced lncRNA LOC105374902 promotes the malignant behavior of cervical cancer cells by acting as a sponge of miR-1285-3p.

Biochemical and biophysical research communications·2019

Same author

Multi-ancestry genome-wide gene-smoking interaction study of 387,272 individuals identifies new loci associated with serum lipids.

Nature genetics·2019

Same author

Long noncoding RNA CCAT2 promotes hepatocellular carcinoma proliferation and metastasis through up-regulation of NDRG1.

Experimental cell research·2019

Search research articles

Related Experiment Video

Updated: Mar 24, 2026

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

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

Published on: October 28, 2019

ICP4-induced miR-101 attenuates HSV-1 replication.

Xiangling Wang¹, Caifeng Diao¹, Xi Yang¹

¹Tianjin Life Science Research Center and Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, 22 Qi-Xiang-Tai Road, Tianjin 300070, China.

Scientific Reports

|March 18, 2016

Summary

Herpes Simplex Virus type 1 (HSV-1) infection activates the ICP4 gene to induce miR-101, which then suppresses GRSF1, ultimately limiting viral replication and promoting host survival.

More Related Videos

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

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

Published on: November 4, 2018

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

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

Published on: August 24, 2015

Related Experiment Videos

Last Updated: Mar 24, 2026

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

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

Published on: October 28, 2019

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

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

Published on: November 4, 2018

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

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

Published on: August 24, 2015

Area of Science:

Virology
Molecular Biology
Gene Regulation

Background:

Herpes Simplex Virus type 1 (HSV-1) is a DNA virus causing lytic and latent infections.
MicroRNAs (miRNAs) post-transcriptionally regulate gene expression.
Previous studies indicated HSV-1 infection induces miR-101 in HeLa cells.

Purpose of the Study:

To elucidate the mechanism of HSV-1-induced miR-101 expression.
To identify targets of miR-101 involved in HSV-1 replication.
To understand how HSV-1 manipulates host miRNAs for its benefit.

Main Methods:

Investigated the origin of HSV-1-induced miR-101 using its precursor, hsa-mir-101-2.
Examined the interaction of HSV-1 immediate early gene ICP4 with the hsa-mir-101-2 promoter.
Identified G-rich sequence factor 1 (GRSF1) as a miR-101 target and analyzed its role in HSV-1 p40 mRNA regulation.

Main Results:

HSV-1-induced miR-101 is primarily derived from hsa-mir-101-2.
HSV-1 ICP4 directly binds to the hsa-mir-101-2 promoter, activating its expression.
GRSF1 binds to HSV-1 p40 mRNA, enhancing its expression and viral proliferation; miR-101 downregulates GRSF1, attenuating HSV-1 replication.

Conclusions:

HSV-1 ICP4 induces miR-101 expression, which downregulates GRSF1, thereby attenuating viral replication.
This mechanism allows HSV-1 to maintain a permissive host environment by preventing lytic cell death.
The study reveals a novel host-virus interaction where viral genes modulate host miRNAs to regulate defense mechanisms, offering potential antiviral therapeutic targets.