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Seppälä, O.

Publications and source records attributed to Seppälä, O..

2 recordsLinked to original sources

Sublethal immune resistance to parasites generates reaction-norm patterns indistinguishable from tolerance

Hosts defend themselves against parasites through resistance (reducing parasite burden) and tolerance (reducing the fitness cost of infection without affecting parasites). This distinction has important evolutionary implications: resistance is predicted to maintain polymorphism while tolerance tends to fix, and only resistance is expected to provoke parasite counter-adaptation. The reaction-norm framework, which infers tolerance from the slope of host fitness regressed on parasite burden, assumes that a shallow slope reflects parasite-independent host protection. We test this assumption using a within-host model in two variants: microparasites (Model 1, with within-host replication) and macroparasites (Model 2, without). Sublethal immunity impairs the parasites host-exploitation rate, reducing both growth and per-parasite virulence without killing them. We show that this generates systematic slope differences among host genotypes that the framework interprets as variation in tolerance. Furthermore, the ranking of genotypes slopes reverses between linear and sigmoidal damage functions: under linear damage, the strongest immune responder appears most tolerant; under sigmoidal damage, the weakest responder does. Decomposition of the damage reduction shows that virulence reduction accounts for the majority of the effect across both model variants. Thus, the reaction-norm slope cannot determine whether host fitness is maintained by parasite-independent tissue protection or by sublethal impairment of parasites.

evolutionary biology↗

Intraspecific genetic variation modulates immune responses to acute heat exposure in an aquatic ectotherm

Climate change-induced heatwaves threaten ectotherms, whose physiology is tightly coupled to ambient temperature. Vulnerability assessments often rely on data from one or a few populations, implicitly assuming uniform thermal sensitivity across species genetic diversity. Quantifying such variation is especially important for traits with wider ecological consequences; our focus here is on immune function, which shapes disease dynamics. We addressed this knowledge gap using ten clonal lineages of the New Zealand snail Potamopyrgus antipodarum exposed to ambient (17{degrees}C) or heatwave conditions (27{degrees}C) for 4 or 8 days. We measured two complementary innate immune traits: general phenoloxidase-like (PO-like) activity, which integrates the activity of multiple phenoloxidase enzymes, and laccase activity, which targets a specific PO enzyme subclass important in mollusc immunity. Heat exposure suppressed both traits, but patterns differed across clones. While PO-like activity declined uniformly, laccase activity showed substantial among-clone variation in heatwave responses at day 4, though these differences converged by day 8. Heat-induced immune suppression is thus trait-specific, depends on genetic background, and varies with exposure duration. Together, these results demonstrate that studies limited to a single genotype, population, or timepoint risk miscalculating species-level vulnerability.

physiology↗