The RNAi pathway plays a small part in Wolbachia-mediated blocking of dengue virus in mosquito cells

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Reproducible dsRNA Microinjection and Oviposition Bioassay in Mosquitoes and House Flies

Published on: November 8, 2018

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Gerard Terradas1, D Albert Joubert2, Elizabeth A McGraw1

  • 1School of Biological Sciences, Monash University, Clayton VIC 3800, Melbourne, Australia.

Scientific Reports
|March 7, 2017
PubMed

Insights

Wolbachia bacteria reduce dengue virus in mosquitoes by activating immune genes. Suppressing RNAi, a key immune pathway, partially restored dengue virus replication, indicating its role in Wolbachia-mediated protection.

Area of Science:

  • Microbiology
  • Virology
  • Immunology

Background:

  • Wolbachia pipientis is an insect endosymbiont that limits dengue and Zika virus replication in Aedes aegypti mosquitoes.
  • Global Wolbachia releases aim to control mosquito-borne viral diseases.
  • Theories suggest Wolbachia protects mosquitoes via immune priming or resource competition.

Purpose of the Study:

  • To investigate the role of innate immune pathways in Wolbachia-mediated dengue virus control.
  • To determine if targeting specific immune pathways affects dengue virus loads in Wolbachia-infected cells.

Main Methods:

  • Utilized an Aedes aegypti cell line infected with Wolbachia.
  • Employed targeted small interfering RNAs (siRNAs) to reduce expression of major innate immune pathways.
  • Quantified dengue virus (DENV) loads following siRNA treatment.

Main Results:

  • Wolbachia infection upregulated genes in the Toll, JAK/STAT, and RNAi immune pathways.
  • Reducing RNAi pathway gene expression led to a partial rebound of DENV loads in Wolbachia-infected cells.
  • The effect of RNAi suppression accounted for less than 10% of the total DENV load.

Conclusions:

  • The RNAi pathway plays a role in Wolbachia-mediated dengue virus control in Aedes aegypti.
  • Other factors, beyond RNAi expression, are critical for complete dengue virus blocking.
  • Findings suggest the long-term stability of Wolbachia-based disease control strategies due to immune gene plasticity.

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