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Updated: Nov 3, 2025

RNAi-mediated Gene Knockdown and In Vivo Diuresis Assay in Adult Female Aedes aegypti Mosquitoes
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Juvenile Hormone-Sensitive Ribosomal Activity Enhances Viral Replication in Aedes aegypti

Zuo-Kun Shi1,2, Dan Wen1,2, Meng-Meng Chang1,2

  • 1State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.

Msystems
|June 1, 2021
PubMed

Insights

Zika virus (ZIKV) infection in Aedes aegypti mosquitoes is modulated by leucine-rich immune proteins and ribosomal genes. Silencing these factors enhances mosquito resistance, suggesting a novel strategy to control ZIKV transmission.

Area of Science:

  • * Vector-borne disease research
  • * Mosquito immunology
  • * Arthropod-borne viral infections

Background:

  • * Zika virus (ZIKV) is transmitted by the Aedes aegypti mosquito, with poorly understood vector-virus interactions.
  • * Existing treatments for ZIKV are limited, necessitating strategies to reduce vector competence.

Purpose of the Study:

  • * To elucidate the molecular mechanisms underlying ZIKV infection in A. aegypti.
  • * To identify host factors in mosquitoes that can be targeted to control ZIKV transmission.

Main Methods:

  • * RNA interference (RNAi) gene silencing of immune and ribosomal genes in A. aegypti.
  • * Transcriptome analysis to assess gene expression changes upon ZIKV infection.
  • * Quantitative analysis of ZIKV load in mosquitoes.
  • * In vitro fat body culture assays to investigate gene regulation by Juvenile hormone (JH).

Main Results:

  • * Immunity-related genes, including leucine-rich immune protein (LRIM) genes, were upregulated during ZIKV infection.
  • * Silencing of LRIM9, LRIM10A, and LRIM10B genes significantly increased ZIKV load, indicating their antiviral role.
  • * ZIKV infection increased ribosomal activity, with silencing of ribosomal genes RpL23 and RpL27 enhancing mosquito resistance.
  • * RpL23 and RpL27 expression is regulated by the Juvenile hormone (JH) signaling pathway via the methoprene-tolerant (Met) receptor.
  • * Silencing of Met also inhibited ZIKV infection.

Conclusions:

  • * ZIKV manipulates the mosquito's JH signaling pathway to enhance ribosomal activity and promote infection.
  • * LRIM genes play a role in A. aegypti's defense against ZIKV.
  • * Targeting JH-regulated ribosomal genes presents a novel strategy to reduce ZIKV vector competence and transmission.
Keywords:
LRIMantiviraljuvenile hormonemosquitoribosome

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