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Complex interaction between dengue virus replication and expression of miRNA-133a
Jorge Andrés Castillo1, Juan Camilo Castrillón1, Mayra Diosa-Toro1,2
1Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia UdeA, Calle 70 No. 52-21, Medellin, Colombia.
BMC Infectious Diseases
|January 29, 2016
Summary
MicroRNA-133a suppresses dengue virus (DENV) replication by targeting the viral genome and down-regulating host factor PTB. This suggests miRNA-133a may be a potential therapeutic target against DENV infection.
Area of Science:
- Virology
- Molecular Biology
- Genetics
Background:
- Dengue virus (DENV) is a major global health threat, causing millions of infections annually.
- MicroRNAs (miRNAs) are key regulators of gene expression with known antiviral roles, but their specific involvement in DENV replication remains unclear.
Purpose of the Study:
- To investigate the relationship between cellular microRNAs and DENV replication.
- To determine the role of miRNA-133a in DENV replication and its potential targets within the virus or host cells.
Main Methods:
- Bioinformatic analysis to identify potential miRNA targets in the DENV genome.
- Overexpression of miRNA-133a in Vero cells to assess its effect on DENV replication.
- RT-qPCR and Taqman miRNA assays to profile miRNA and PTB expression.
- Western blot analysis to evaluate PTB protein levels.
Main Results:
- Bioinformatic analysis identified the DENV 3'UTR as a target for multiple cellular miRNAs, including miRNA-133a.
- Overexpression of miRNA-133a significantly suppressed DENV replication in Vero cells.
- DENV infection led to down-regulation of PTB, a known miRNA-133a target, suggesting a feedback mechanism where DENV down-regulates miRNA-133a.
Conclusions:
- miRNA-133a plays a regulatory role in DENV replication, potentially by targeting host factors like PTB.
- Further in vivo studies are warranted to confirm the anti-DENV potential of miRNA-133a.
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