Abstract
Synthetic pesticides are now obsolete and alternative solutions are needed to control arthropod populations that are pests and disease vectors. Our team is interested in the interactions between the Junonia coenia densovirus (JcDV, ambidensovirus 1) and the plant-eating Lepidoptera Spodoptera frugiperda. We have shown in this study model that JcDV, when ingested by the larva, crosses by trancytosis the intestinal epithelium (Wang et al., J. Virol, 2013) before replicating in its target tissues (tracheae, hemocytes). Upstream of the intestinal epithelium, the first barrier that the virus must cross is the peritrophic matrix (PM), α-chitin polymer associated with glycosylated proteins that protects the insect from abrasion and pathogens like mucus in other organisms. The viral particles ingested by the larva are concentrated on this matrix. Our first goal was to understand how the virus crosses the PM. By basing our strategy on the competition between the virus and free glycans, essentially the major component of chitin N-acetyl glucosamine (GlcNAc), we have shown in vitro, ex vivo and in vivo that the interaction of the virus with glycans is essential to the infection, which is however more effective when the virus is only semi-purified. This led us to look for specific PM virus ligands. The highly glycosylated proteins, also some low glycosylated proteins that are recognized by the virus, are undergoing proteomic analysis. In particular, we will try to identify the PM protein (s) whose interaction with JcDV may explain the destruction of the PM observed during the infection. We also started a transcriptomic analysis of the infected vs. uninfected gut to understand GlcNAc synthesis arrest 24h post-infection. Finally, we began a similar work on the interaction between JcDV and the lipid rafts of the midgut brush border of the S. frugiperda larva.