Abstract
Variation in susceptibility to infection has a substantial genetic component in natural populations, and it has been argued that selection by pathogens may result in it having a simpler genetic architecture than many other quantitative traits. This is important as models of host–pathogen co‐evolution typically assume resistance is controlled by a small number of genes. Using the Drosophila melanogaster multiparent advanced intercross, we investigated the genetic architecture of resistance to two naturally occurring viruses, the sigma virus and DCV (Drosophila C virus). We found extensive genetic variation in resistance to both viruses. For DCV resistance, this variation is largely caused by two major‐effect loci. Sigma virus resistance involves more genes – we mapped five loci, and together these explained less than half the genetic variance. Nonetheless, several of these had a large effect on resistance. Models of co‐evolution typically assume strong epistatic interactions between polymorphisms controlling resistance, but we were only able to detect one locus that altered the effect of the main effect loci we had mapped. Most of the loci we mapped were probably at an intermediate frequency in natural populations. Overall, our results are consistent with major‐effect genes commonly affecting susceptibility to infectious diseases, with DCV resistance being a near‐Mendelian trait.
Highlights
Variation in susceptibility to infectious disease often has a substantial genetic component in natural populations, including plants (Thompson & Burdon 1992), invertebrates (Lazzaro et al 2004; Bennett et al 2005) and humans (Cooke & Hill 2001)
We found extensive genetic variation in resistance to two viruses that naturally infect D. melanogaster in the wild
For DCV the genetic architecture was near-Mendelian, we identified a major-effect locus that increased survival times by about 81% and explained 77.8% of the genetic variation in resistance and another large-effect quantitative trait locus (QTL) that led to 39% increase in survival times and explained 11.3% of the genetic variation
Summary
Variation in susceptibility to infectious disease often has a substantial genetic component in natural populations, including plants (Thompson & Burdon 1992), invertebrates (Lazzaro et al 2004; Bennett et al 2005) and humans (Cooke & Hill 2001). Because pathogens are an important selective force in the wild, there is probably to be strong natural selection on this variation in populations This can be positive selection that drives resistance alleles through fixation (Woolhouse et al 2002; Bangham et al 2007; Magwire et al 2011). Most theoretical attention has been paid to models in which co-evolution between hosts and pathogens results in negative frequency-dependent selection that can maintain both
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