Abstract
It is common to find abundant genetic variation in host resistance and parasite infectivity within populations, with the outcome of infection frequently depending on genotype-specific interactions. Underlying these effects are complex immune defenses that are under the control of both host and parasite genes. We have found extensive variation in Drosophila melanogaster’s immune response against the parasitoid wasp Leptopilina boulardi. Some aspects of the immune response, such as phenoloxidase activity, are predominantly affected by the host genotype. Some, such as upregulation of the complement-like protein Tep1, are controlled by the parasite genotype. Others, like the differentiation of immune cells called lamellocytes, depend on the specific combination of host and parasite genotypes. These observations illustrate how the outcome of infection depends on independent genetic effects on different aspects of host immunity. As parasite-killing results from the concerted action of different components of the immune response, these observations provide a physiological mechanism to generate phenomena like epistasis and genotype-interactions that underlie models of coevolution.
Highlights
When a host is exposed to a parasite, the likelihood of infection and the subsequent severity of disease are frequently affected by both the host and parasite genotypes
Resistance frequently depends on the combination of host and parasite genomes—a host which is resistant to one parasite genotype may be susceptible to a different genotype
To understand how differences in the immune response give rise to these genetic interactions, we have studied a parasitic wasp that lays its eggs within the larvae of the fruit fly Drosophila melanogaster
Summary
When a host is exposed to a parasite, the likelihood of infection and the subsequent severity of disease are frequently affected by both the host and parasite genotypes. The outcome of infection depends on the combination of host and parasite genotypes, such that the susceptibility of a host to one parasite genotype does not predict its susceptibility to a different parasite genotype [1]. The success of an infection is frequently determined by the host immune response These are complex traits that are typically comprised of cellular processes, such as phagocytosis, and humoral processes, such as production of antimicrobial peptides [4]. Genetic variation affecting the outcomes of infection, such as infectivity, pathogen load or disease severity, is likely the result of multiple independent effects on different aspects of the immune response or other traits
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