Dissemin is shutting down on January 1st, 2025

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National Academy of Sciences, Proceedings of the National Academy of Sciences, 46(109), p. 18915-18920, 2012

DOI: 10.1073/pnas.1205231109

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Secreted Vago restricts West Nile virus infection in Culex mosquito cells by activating the Jak-STAT pathway

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

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 ( Cx Vago) is up-regulated in response to WNV infection in a Dicer-2–dependent manner. Further, our data show that Cx Vago 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.