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Dynamic Interplay Between miR-133a and RBMX During Dengue Virus Infection
Anjali Singh1, Saumya Sinha1, Bhupendra Verma1
1Department of Biotechnology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India.
Journal of Medical Virology
|August 7, 2025
Summary
Dengue virus infection alters RBMX protein and miR-133a levels. miR-133a acts as an antiviral by targeting RBMX, revealing a key regulatory axis in dengue pathogenesis.
Area of Science:
- Molecular Virology
- RNA Biology
- Host-Pathogen Interactions
Background:
- Viruses depend on host cells for replication.
- Dengue virus (DENV) infection impacts host gene expression.
- RNA-binding proteins (RBPs) and microRNAs (miRNAs) are crucial in viral infections.
Purpose of the Study:
- To investigate the interplay between RBMX, miR-133a, and DENV infection.
- To elucidate the regulatory mechanisms governing RBMX and miR-133a during DENV pathogenesis.
- To explore the potential of targeting this axis for antiviral strategies.
Main Methods:
- Analysis of RBMX and miR-133a expression in infected cells.
- Bioinformatic prediction (Targetscan) and luciferase assays to confirm miRNA-target interaction.
- Time-point studies using miR-133a mimics and inhibitors.
- Immunoprecipitation assays to study DENV 3'UTR interactions.
- RBMX overexpression studies in ivermectin-treated cells.
Main Results:
- DENV infection upregulates RBMX and downregulates miR-133a.
- miR-133a directly targets RBMX, suppressing its expression.
- miR-133a exhibits antiviral activity against DENV by targeting RBMX.
- DENV 3'UTR plays a role in regulating RBMX and miR-133a.
- RBMX is vital for DENV replication, and its overexpression partially rescues viral replication in ivermectin-treated cells.
Conclusions:
- A dynamic regulatory axis involving miR-133a and RBMX is modulated during DENV infection.
- miR-133a acts as a host antiviral factor by targeting RBMX.
- Understanding this miRNA/RBP interaction provides insights into DENV pathogenesis and potential therapeutic targets.
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