摘要：SummaryDiseases caused by mosquito-borne viruses have been on the rise for the last decades, and novel methods aiming to use laboratory-engineered mosquitoes that are incapable of carrying viruses have been developed to reduce pathogen transmission. This has stimulated efforts to identify optimal target genes that are naturally involved in mosquito antiviral defenses or required for viral replication. Here, we investigated the role of a member of the Tudor protein family, Tudor-SN, upon dengue virus infection in the mosquitoAedes aegypti.Tudor-SNknockdown reduced dengue virus replication in the midgut ofAe. aegyptifemales. In immunofluorescence assays, Tudor-SN localized to the nucleolus in bothAe. aegyptiandAedes albopictuscells. A reporter assay and small RNA profiling demonstrated that Tudor-SN was not required for RNA interference functionin vivo. Collectively, these results defined a novel proviral role for Tudor-SN upon early dengue virus infection of theAe. aegyptimidgut.Graphical AbstractDisplay OmittedHighlights•Tudor-SNis upregulated in theAe. aegyptimidgut early upon dengue virus infection•Tudor-SNpromotes viral replicationin vitroandin vivo•Tudor-SN localizes to the nucleolus in mosquito cells•Tudor-SNis not required for RNAi functionin vivoGenetics; Virology
