Abstract
Although West Nile virus (WNV) and other arthropod-borne viruses are a major public health problem, the mechanisms of antiviral immunity in mosquitoes are poorly understood. Dicer-2, responsible for the RNAi-mediated response through the C-terminal RNase-III domain, also contains an N-terminal DExD/H-box helicase domain similar to mammalian RIG-I/MDA5 which, in Drosophila, was found to be required for activation of an antiviral gene, Vago. Here we show that the Culex orthologue of Vago (CxVago) is up-regulated in response to WNV infection in a Dicer-2-dependent manner. Further, our data show that CxVago is a secreted peptide that restricts WNV infection by activation of the Jak-STAT pathway. Thus, Vago appears to function as an IFN-like antiviral cytokine in mosquitoes.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Chlorocebus aethiops
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Cricetinae
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Culex / immunology*
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Culex / metabolism
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Culex / virology
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Cytokines / immunology*
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Cytokines / metabolism
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DEAD-box RNA Helicases / immunology
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DEAD-box RNA Helicases / metabolism
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Drosophila melanogaster
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Humans
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Immunity, Innate / physiology*
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Insect Proteins / immunology*
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Insect Proteins / metabolism
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Janus Kinases / immunology*
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Janus Kinases / metabolism
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RNA, Viral / immunology
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RNA, Viral / metabolism
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Ribonuclease III / immunology
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Ribonuclease III / metabolism
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STAT Transcription Factors / immunology*
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STAT Transcription Factors / metabolism
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Vero Cells
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West Nile Fever / immunology
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West Nile Fever / metabolism
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West Nile Fever / transmission
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West Nile virus / immunology*
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West Nile virus / metabolism
Substances
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Cytokines
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Insect Proteins
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RNA, Viral
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STAT Transcription Factors
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Janus Kinases
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Ribonuclease III
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DEAD-box RNA Helicases