Abstract
Insects, the most diverse group of animals, can be infected by an extraordinary diversity of viruses. Among them, arthropod-borne viruses can be transmitted to humans, while bee and silkworm viruses cause important economic losses. Like all invertebrates, insects rely solely on innate immunity to counter viral infections. Protein-based mechanisms, involving restriction factors and evolutionarily conserved signaling pathways regulating transcription factors of the NF-kB and STAT families, participate in the control of viral infections in insects. In addition, RNA-based responses play a major role in the silencing of viral RNAs. We review here our current state of knowledge on insect antiviral defense mechanisms, which include conserved as well as adaptive, insect-specific strategies. Identification of the innate immunity receptors that sense viral infection in insects remains a major challenge for the field.
Highlights
With more than 1 million known species, insects are the largest group of multicellular organisms, representing over 70% of animal species
Insects are exposed to a large panel of infectious microorganisms, which they control through their innate immune system (Hoffmann et al, 1999)
This study revealed that much of the diversity of negative-sense RNA viruses found in plants and vertebrate animals falls within the genetic diversity of viruses associated with arthropods (Dudas and Obbard, 2015; Li et al, 2015)
Summary
With more than 1 million known species, insects are the largest group of multicellular organisms, representing over 70% of animal species. Pointing to an involvement of components of the IMD pathway in antiviral immunity, in Culex mosquitoes, a Dicer-2-dependent pathway regulates caister.com/cimb expression of the gene Vago upon activation of a TRAF factor and the homologue of Relish, REL2 (Paradkar et al, 2014). It appears that NF-κB pathways are more diverse than initially thought, and that these evolutionarily conserved transcription factors can be activated by alternative branches of the canonical Toll and IMD pathways initially characterized in the context of bacterial and fungal infections. The RISC will slice the mRNA target and release the degradation product in an ATP assisted manner
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