Insect-specific virus evolution and potential effects on vector competence

Abstract

The advancement in high-throughput sequencing technology and bioinformatics tools has spurred a new age of viral discovery. Arthropods is the largest group of animals and has shown to be a major reservoir of different viruses, including a group known as insect-specific viruses (ISVs). The majority of known ISVs have been isolated from mosquitoes and shown to belong to viral families associated with animal arbovirus pathogens, such as Flaviviridae, Togaviridae and Phenuiviridae. These insect-specific viruses have a strict tropism and are unable to replicate in vertebrate cells, these properties are interesting for many reasons. One is that these viruses could potentially be utilised as biocontrol agents using a similar strategy as for Wolbachia. Mosquitoes infected with the viral agent could have inferior vectorial capacity of arboviruses resulting in a decrease of circulating arboviruses of public health importance. Moreover, insect-specific viruses are thought to be ancestral to arboviruses and could be used to study the evolution of the switch from single-host to dual-host. In this review, we discuss new discoveries and hypothesis in the field of arboviruses and insect-specific viruses.

Keywords: Arbovirus; Evolution; Insect-specific virus; Vector competence.

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