| dc.description.abstract | The intracellular bacterium Wolbachia pipientis is widely spread amongst insect populations, like Drosophila.
Recently, Wolbachia infection was found to reduce virus-induced mortality and lower the viral load in dually
infected Drosophila melanogaster. Unravelling the mechanism behind this Wolbachia-induced survival might further
elucidate the high prevalence of Wolbachia amongst insect species; but above all it might give new insights in
antiviral immunity of insects that spread vector-borne diseases and it might help to better understand antiviral
immunity in general. Even thought Wolbachia infection does not induce a clear phenotype in D. melanogaster, it
does result in profound changes in transcription, for example of signaling molecules in the Toll, Imd, and JNK
pathways. In addition, heat shock proteins, autophagy, and other processes – possibly induced by secreted
Ankyrin-repeat-containing proteins of Wolbachia – might be active during Wolbachia infection. Wolbachia was
shown to protect against positive sense (+) single-stranded RNA viruses from different families that replicate in
association with cellular membranes. These viruses normally promote antiviral RNA interference, Imd and
Jak/STAT signaling, autophagy, phagocytosis, and/or apoptosis in Drosophila. Remarkably, Wolbachia does not
protect against infection with a double-stranded DNA virus. Unfortunately, little is known about the reactions
induced upon double-stranded DNA-virus infection. All together, Wolbachia might protect Drosophila by priming
the antiviral immune response, for example by activating Imd and Toll signaling. Importantly, all examined RNA
viruses show overlapping cell tropism with Wolbachia, thus Wolbachia might also directly affect viral replication.
For example, Wolbachia could slow down viral replication by competing for cellular nutrients, affect vesicle
transport, or secrete proteins detrimental to the viruses. Additional research will unravel the mechanism behind
the Wolbachia-induced antiviral immunity in Drosophila and the occurrence of this phenomenon amongst other
species. | |
