Parasites are thought to be a major driving force shaping genetic variation in their host, and are suggested to be a significant reason for the maintenance of sexual reproduction. A leading hypothesis for the occurrence of multiple mating (polyandry) in social insects is that the genetic diversity generated within-colonies through this behavior promotes disease resistance. This benefit is likely to be particularly significant when colonies are exposed to multiple species and strains of parasites, but host–parasite genotypic interactions in social insects are little known. We investigated this using honey bees, which are naturally polyandrous and consequently produce genetically diverse colonies containing multiple genotypes (patrilines), and which are also known to host multiple strains of various parasite species. We found that host genotypes differed significantly in their resistance to different strains of the obligate fungal parasite that causes chalkbrood disease, while genotypic variation in resistance to the facultative fungal parasite that causes stonebrood disease was less pronounced. Our results show that genetic variation in disease resistance depends in part on the parasite genotype, as well as species, with the latter most likely relating to differences in parasite life history and host–parasite coevolution. Our results suggest that the selection pressure from genetically diverse parasites might be an important driving force in the evolution of polyandry, a mechanism that generates significant genetic diversity in social insects.

-The genetic basis of host resistance to parasites is a fundamental aspect of host-parasite co-evolution, yet the precise mechanisms often remain unclear. Here, we follow on from a previous study on the genetically mediated variation in resistance to two common fungal brood parasites that cause chalkbrood and stonebrood in the honey bee. We assessed whether genetically mediated variation in resistance can be explained by the baseline immunocompetence of different larval genotypes by correlating the constitutive expression of two key immune genes with the observed level of resistance of each larval genotype to four different fungal brood parasites. We found significant variation between larval genotypes in the constitutive expression of abaecin but not defensin 2 , but despite a suggestion of negative correlations between gene expression and resistance level in older larvae, there was no consistent evidence that baseline abaecin expression is a relevant predictor of resistance to these parasites. These results suggest that the constitutive expression of abaecin appears to have a genetic basis in honey bee larvae but that mechanisms other than innate expression of antimicrobial peptides might be more important in defence against the specific fungal brood parasites assessed here.Apis mellifera / abaecin / defensin / antimicrobial peptide / Ascosphaera apis / Aspergillus flavus

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