An evolutionary conserved function of the JAK-STAT pathway in anti-dengue defense

Jayme A. Souza-Neto, Shuzhen Sim, George Dimopoulos

Research output: Contribution to journalArticle

Abstract

Here, we show that the major mosquito vector for dengue virus uses the JAK-STAT pathway to control virus infection. Dengue virus infection in Aedes aegypti mosquitoes activates the JAK-STAT immune signaling pathway. The mosquito's susceptibility to dengue virus infection increases when the JAK-STAT pathway is suppressed through RNAi depletion of its receptor Domeless (Dome) and the Janus kinase (Hop), whereas mosquitoes become more resistant to the virus when the negative regulator of the JAK-STAT pathway, PIAS, is silenced. The JAK-STAT pathway exerts its anti-dengue activity presumably through one or several STAT-regulated effectors. We have identified, and partially characterized, two JAK-STAT pathway-regulated and infection-responsive dengue virus restriction factors (DVRFs) that contain putative STAT-binding sites in their promoter regions. Our data suggest that the JAK-STAT pathway is part of the A. aegypti mosquito's antidengue defense and may act independently of the Toll pathway and the RNAi-mediated antiviral defenses.

Original languageEnglish (US)
Pages (from-to)17841-17846
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume106
Issue number42
DOIs
StatePublished - Oct 20 2009

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Dengue Virus
Dengue
Culicidae
Virus Diseases
RNA Interference
Janus Kinases
Humulus
Aedes
Genetic Promoter Regions
Antiviral Agents
Binding Sites
Viruses
Infection

Keywords

  • Aedes aegypti
  • Dengue fever
  • Innate immunity
  • Resistance
  • Transcriptome

ASJC Scopus subject areas

  • General

Cite this

An evolutionary conserved function of the JAK-STAT pathway in anti-dengue defense. / Souza-Neto, Jayme A.; Sim, Shuzhen; Dimopoulos, George.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 106, No. 42, 20.10.2009, p. 17841-17846.

Research output: Contribution to journalArticle

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