Abstract
Pathogen entry route can have a strong impact on the result of microbial infections in different hosts, including insects. Drosophila melanogaster has been a successful model system to study the immune response to systemic viral infection. Here we investigate the role of the Toll pathway in resistance to oral viral infection in D. melanogaster. We show that several Toll pathway components, including Spätzle, Toll, Pelle and the NF-kB-like transcription factor Dorsal, are required to resist oral infection with Drosophila C virus. Furthermore, in the fat body Dorsal is translocated from the cytoplasm to the nucleus and a Toll pathway target gene reporter is upregulated in response to Drosophila C Virus infection. This pathway also mediates resistance to several other RNA viruses (Cricket paralysis virus, Flock House virus, and Nora virus). Compared with control, viral titres are highly increased in Toll pathway mutants. The role of the Toll pathway in resistance to viruses in D. melanogaster is restricted to oral infection since we do not observe a phenotype associated with systemic infection. We also show that Wolbachia and other Drosophila-associated microbiota do not interact with the Toll pathway-mediated resistance to oral infection. We therefore identify the Toll pathway as a new general inducible pathway that mediates strong resistance to viruses with a route-specific role. These results contribute to a better understanding of viral oral infection resistance in insects, which is particularly relevant in the context of transmission of arboviruses by insect vectors.
Highlights
Pathogens can infect their hosts through many different routes
We found that Drosophila C virus (DCV) oral infection in adult DrosDel w1118 isogenic [52] flies can cause a lethal infection in both females and males, killing up to 25% of flies in 20 days (Fig. 1A, 1B and Dataset S1)
As with DCV oral infections, we found that a greater number of pll mutant flies exhibited higher amounts of Cricket Paralysis virus (CrPV) RNA when compared with w1118 iso flies (Fig. 6B and Dataset S14). plldeficient flies showed the same susceptibility to CrPV systemic infection as control flies at different viral infection titres (Fig. 6C, S9B and Dataset S15)
Summary
Pathogens can infect their hosts through many different routes. For instance, microbes can directly enter the host through skin lesions or mediated by insect vectors. Most of human infections start at mucosal surfaces of the respiratory, digestive or genital tracts. Pathogens specialize in different transmission strategies involving different host tissues. Hosts mount distinct immune responses in different tissues, involving specialized cells and structures. Pathogen entry route can have a strong impact on the result of infection in animals, from humans to insects [1,2,3,4]
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