Abstract
ABSTRACT
Understanding the genetic architecture of pathogen resistance and its relationship to host life‐history traits is a fundamental problem in evolutionary biology, yet the conditions under which resistance costs manifest as detectable trade‐offs remain poorly understood. Here, we examine resistance in
Plodia interpunctella
(Indian meal moth) to its granulovirus (PiGV) across 12 inbred lines maintained without deliberate pathogen exposure, alongside an independently assembled outbred stock population as a genomic reference. We quantify resistance using LD50 values from dose–response assays, summarize developmental life‐history variation using a composite principal‐component axis derived from pupal weight, development time and growth rate, and evaluate genomic structure and window‐level associations with resistance. Resistance varied approximately two‐fold across inbred lines. Neither the composite life‐history axis nor any individual life‐history trait was significantly correlated with LD50. In contrast, genomic PC1, the primary axis of CDS‐restricted genomic differentiation, was significantly associated with resistance (
r
= −0.65,
p
= 0.022), whereas overall pairwise distance was not. No individual PCA‐LD50 window survived multiple‐testing correction; instead, resistance‐associated signal was distributed broadly across the genome, and convergent signal spanning five chromosomes showed no enrichment for genes with known immune functions. This pattern is consistent with a diffuse, potentially polygenic basis for resistance, although the modest number of lines limits locus‐level inference. Together with prior work demonstrating resistance‐growth trade‐offs in this system, our results suggest that resistance can be genomically structured without detectable coupling to the developmental life‐history variation measured here, and that expression of resistance costs depends on genetic and environmental context.