RT Journal Article
SR Electronic
T1 Insulin potentiates JAK/STAT signaling to broadly inhibit flavivirus replication in insect vectors
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 701714
DO 10.1101/701714
A1 Laura R.H. Ahlers
A1 Chasity E. Trammell
A1 Grace F. Carrell
A1 Sophie Mackinnon
A1 Brandi K. Torrevillas
A1 Clement Y. Chow
A1 Shirley Luckhart
A1 Alan G. Goodman
YR 2019
UL http://biorxiv.org/content/early/2019/07/13/701714.abstract
AB The World Health Organization estimates that over half of the world’s population is at risk for vector-borne diseases, such as those caused by arboviral infection. Because many arboviruses are mosquito-borne, investigation of the insect immune response will help identify targets that could reduce the spread of these viruses by the mosquito. In this study, we used a genetic screening approach to identify insulin-like receptor as a novel component of the immune response to arboviral infection. We determined that vertebrate insulin reduces West Nile virus (WNV) replication in Drosophila melanogaster as well as WNV, Zika, and dengue virus titers in mosquito cells. Mechanistically, we showed that insulin signaling activates the JAK/STAT, but not RNAi, pathway to control infection. Finally, we validated that insulin priming of adult female Culex mosquitoes through a blood meal reduces WNV infection, demonstrating an essential role for insulin signaling in insect antiviral responses to emerging human pathogens.