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BMC Infect Dis. 2016 Jan 27;16:29. doi: 10.1186/s12879-016-1364-y.

Complex interaction between dengue virus replication and expression of miRNA-133a.

Author information

1
Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia UdeA, Calle 70 No. 52-21, Medellin, Colombia.
2
Department of Medical Microbiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
3
St Laurent Institute, 317 New Boston St, Woburn, MA, 01801, USA.
4
Grupo Inmunovirología, Facultad de Medicina, Universidad de Antioquia UdeA, Calle 70 No. 52-21, Medellin, Colombia. Silvio.urcuqui@udea.edu.co.

Abstract

BACKGROUND:

Dengue virus (DENV) is the most common vector-borne viral infection worldwide with approximately 390 million cases and 25,000 reported deaths each year. MicroRNAs (miRNAs) are small non-coding RNA molecules responsible for the regulation of gene expression by repressing mRNA translation or inducing mRNA degradation. Although miRNAs possess antiviral activity against many mammalian-infecting viruses, their involvement in DENV replication is poorly understood.

METHODS:

Here, we explored the relationship between DENV and cellular microRNAs using bioinformatics tools. We overexpressed miRNA-133a in Vero cells to test its role in DENV replication and analyzed its expression using RT-qPCR. Furthermore, the expression of polypyrimidine tract binding protein (PTB), a protein involved in DENV replication, was analyzed by western blot. In addition, we profiled miRNA-133a expression in Vero cells challenged with DENV-2, using Taqman miRNA.

RESULTS:

Bioinformatic analysis revealed that the 3' untranslated region (3'UTR) of the DENV genome of all four DENV serotypes is targeted by several cellular miRNAs, including miRNA-133a. We found that overexpression of synthetic miRNA-133a suppressed DENV replication. Additionally, we observed that PTB transcription , a miRNA-133a target, is down-regulated during DENV infection. Based in our results we propose that 3'UTR of DENV down-regulates endogenous expression of miRNA-133a in Vero cells during the first hours of infection.

CONCLUSIONS:

miRNA-133a regulates DENV replication possibly through the modulation of a host factor such as PTB. Further investigations are needed to verify whether miRNA-133a has an anti-DENV effect in vivo.

PMID:
26818704
PMCID:
PMC4728791
DOI:
10.1186/s12879-016-1364-y
[Indexed for MEDLINE]
Free PMC Article

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