It is common to find considerable genetic variation in susceptibility to infection in natural populations. To investigate whether natural selection increases this variation we tested whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. Check out the paper in eLIFE here.
In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. This was an epic experiment, and a huge team effort, taking nearly 7 years and involving injecting >70,000 flies (kudos to Jon Day injection machine!).
We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-pathogen interactions. It seems likely that selection by pathogens has increased genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.
A major source of emerging infectious disease is pathogens jumping into novel hosts where they have no co-evolutionary history. Our results suggest that when a pathogen infects a novel host species, there may be far less genetic variation in susceptibility among individuals than is normally the case. This may create a ‘monoculture effect’ (King and Lively, 2012; Lively, 2010; Ostfeld and Keesing, 2012), which could leave populations vulnerable to epidemics of pathogens that have previously circulated in other host species. Longer term, low levels of pre-standing genetic variation may slow down the rate at which the new host can evolve resistance to a new pathogen.
Ben Longdon 