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Related Experiment Video

Updated: Jun 4, 2026

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

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MiR-101 regulates HSV-1 replication by targeting ATP5B.

Shu-qi Zheng¹, Yi-xuan Li, Yan Zhang

¹Tianjin Life Science Research Center and Basic Medical School, Tianjin Medical University, China.

Antiviral Research

|February 5, 2011

Summary

MicroRNAs (miRNAs) regulate gene expression and impact viral infections. This study shows miR-101 suppresses herpes simplex virus-1 (HSV-1) replication by targeting ATP5B, a pro-viral factor.

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Area of Science:

Molecular Biology
Virology
Gene Regulation

Background:

MicroRNAs (miRNAs) are key regulators of gene expression.
Host-pathogen interactions involve complex molecular crosstalk.
Herpes simplex virus-1 (HSV-1) is a significant human pathogen.

Purpose of the Study:

To investigate the role of miR-101 in HSV-1 replication.
To identify the molecular targets of miR-101 during HSV-1 infection.
To elucidate the mechanism by which miR-101 affects viral replication.

Main Methods:

Plaque assays and real-time PCR to quantify viral replication.
Bioinformatics analysis to predict miRNA-target interactions.
RNA interference and ectopic expression to study gene function.

Main Results:

Ectopic miR-101 expression suppressed HSV-1 replication.
Blocking endogenous miR-101 enhanced viral progeny.
MiR-101 directly targets the 3' UTR of ATP5B, inhibiting its expression.
ATP5B knockdown inhibited HSV-1 replication, identifying it as a pro-viral factor.
An inverse correlation between miR-101 and ATP5B was observed in infected cells.

Conclusions:

miR-101 plays a critical role in suppressing HSV-1 replication.
Targeting ATP5B is a key mechanism for miR-101's antiviral activity.
Understanding host miRNA-virus interactions enhances knowledge of host-pathogen dynamics.