Tudor-SN Promotes Early Replication of Dengue Virus in the Aedes aegypti Midgut

Sarah Hélène Merkling (1) , Vincent Raquin (1) , Stéphanie Dabo (1) , Annabelle Henrion-Lacritick (2) , Hervé Blanc (2) , Isabelle Moltini-Conclois (1) , Lionel Frangeul (2) , Hugo Varet (3, 4) , Maria-Carla P Saleh (2) , Louis Lambrechts (1)

1 IVI - Interactions Virus-Insectes - Insect-Virus Interactions
2 Virus et Interférence ARN - Viruses and RNA Interference
3 Hub Bioinformatique et Biostatistique - Bioinformatics and Biostatistics HUB
4 Biomics (plateforme technologique)

Diseases 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 mosquito Aedes aegypti. Tudor-SN knockdown reduced dengue virus replication in the midgut of Ae. aegypti females. In immunofluorescence assays, Tudor-SN localized to the nucleolus in both Ae. aegypti and Aedes albopictus cells. A reporter assay and small RNA profiling demonstrated that Tudor-SN was not required for RNA interference function in vivo. Collectively, these results defined a novel proviral role for Tudor-SN upon early dengue virus infection of the Ae. aegypti midgut.

Keywords: Virology; Genetics

Domains: Life Sciences [q-bio]; Life Sciences [q-bio]; Microbiology and Parasitology; Virology; Life Sciences [q-bio]; Genetics

Sarah Hélène Merkling, Vincent Raquin, Stéphanie Dabo, Annabelle Henrion-Lacritick, Hervé Blanc, et al.. Tudor-SN Promotes Early Replication of Dengue Virus in the Aedes aegypti Midgut. iScience, 2020, 23 (2), pp.100870. ⟨10.1016/j.isci.2020.100870⟩. ⟨pasteur-02562446⟩