Fig. 1.

Schematic overview of some of the mosquito antiviral mechanisms. a The mosquito ingests an arbovirus-infectious blood meal into the midgut. The virus enters and replicate in the midgut epithelial cells, after successful replication the virus escape into the haemolymph and spread systemically including to the salivary glands, where the virus enters and replicate before being transmitted via the saliva. b The JAK-STAT pathway is mainly activated when the transmembrane receptor Domeless (Dome) recognise extracellular unpaired ligands (Upd) leading to a conformational change that start autophosphorylation of Hop, which in turn phosphorylates Dome. This is leads to the phosphorylation and dimerization of STAT, resulting in a translocation of STAT dimers to the nucleus which activates the transcription of specific antiviral genes. c A primary viral infection can block a secondary infection of a similar virus via mechanisms hypothesised to involve competition for, or modification of cellular resources reducing receptor binding, viral entry, RNA replication and translation of the secondary virus. d Viral dsRNA, either as replication intermediates or as part of the viral genomes, are processed by the Dcr-2-R2D2 complex to generate siRNAs of approximately 21–23 bp of length. The siRNA are incorporated into the RNA-induced silencing complex (RISC) to recognize viral RNA for degradation. dsRNA can be sensed by the Dicer-2 DEcD/H-box helicase domain and via an unknown pathway activate expression and secretion of Vago, which can activate the JAK-STAT pathway via an unknown receptor in nearby cells