Darren J. Obbard
Research FellowUniversity of Edinburgh
Institute of Evolutionary Biology
Centre for immunity, Infection, and Evolution
Ashworth Labs, Kings Buildings, West Mains Road
Edinburgh, EH9 3JT
United Kingdom
Website
Abstracts (first author)
Discovery, distribution and evolutionary genomics of viruses naturally infecting Drosophila melanogaster
Summary:
Drosophila melanogaster is an important model for innate immunity, and is arguably our primary model for antiviral resistance in arthropods. Several groups have used population-genetic and phylogenetic approaches to show that some antiviral immune genes in Drosophila (notably the antiviral RNAi pathway) display highly elevated rates of adaptive evolution. However, although this is consistent with a host-virus arms race, the evolutionary genetics of Drosophila viruses are almost unstudied - only a handful of viruses which naturally infect Drosophila melanogaster are known, and only Drosophila Sigma Virus (a Rhabdovirus) has been regularly isolated from wild populations.
In an attempt to understand the evolutionary genetics of Drosophila viruses, we have sequenced both RNAseq, and small-RNA, libraries from large pooled samples of wild-caught D. melanogaster. This has allowed us to identify several new viruses, including several RNA viruses (viruses with sequence similarity to Sacbrood Virus, Slow Bee Paralysis Virus, Chronic Bee paralysis virus, Acyrthosiphon Pisum Virus, Flaviviruses, and Cypoviruses) and a DNA virus (Nudivirus).
Following a geographic survey of D. melanogaster, we find that the previously known viruses of D. melanogaster (including DAV, Sigma and Nora) are widespread at low to intermediate prevalence. None of the viruses shows high rates of adaptive evolution, and in general (despite substantial synonymous divergence) protein sequences are very highly conserved. However, while this may indicate that these viruses are not engaged in ‘arms race'-like coevolution, we suspect that the short timescale of viral co-ancestry (tens to hundreds, rather than thousands, of years) makes this process extremely difficult to detect. This is in sharp contrast to viral evolution in response to vertebrate adaptive immunity, which adapts plastically on the same timescale as viral evolution.