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Pathogen evolution under host avoidance plasticity.

ABSTRACT: Host resistance consists of defences that limit pathogen burden, and can be classified as either adaptations targeting recovery from infection or those focused upon infection avoidance. Conventional theory treats avoidance as a fixed strategy which does not vary from one interaction to the next. However, there is increasing empirical evidence that many avoidance strategies are triggered by external stimuli, and thus should be treated as phenotypically plastic responses. Here, we consider the implications of avoidance plasticity for host-pathogen coevolution. We uncover a number of predictions challenging current theory. First, in the absence of pathogen trade-offs, plasticity can restrain pathogen evolution; moreover, the pathogen exploits conditions in which the host would otherwise invest less in resistance, causing resistance escalation. Second, when transmission trades off with pathogen-induced mortality, plasticity encourages avirulence, resulting in a superior fitness outcome for both host and pathogen. Third, plasticity ensures the sterilizing effect of pathogens has consequences for pathogen evolution. When pathogens castrate hosts, selection forces them to minimize mortality virulence; moreover, when transmission trades off with sterility alone, resistance plasticity is sufficient to prevent pathogens from evolving to fully castrate.

SUBMITTER: McLeod DV

PROVIDER: S-EPMC4571713 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Pathogen evolution under host avoidance plasticity.

McLeod David V DV Day Troy T

Proceedings. Biological sciences 20150901 1814

Host resistance consists of defences that limit pathogen burden, and can be classified as either adaptations targeting recovery from infection or those focused upon infection avoidance. Conventional theory treats avoidance as a fixed strategy which does not vary from one interaction to the next. However, there is increasing empirical evidence that many avoidance strategies are triggered by external stimuli, and thus should be treated as phenotypically plastic responses. Here, we consider the imp ...[more]

PMID: 26336170

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Project description:The behavioral immune system posits that disgust functions to protect animals from pathogen exposure. Therefore, cues of pathogen risk should be a primary driver influencing variation in disgust. Yet, to our knowledge, neither the relationship between current pathogen risk and disgust, nor the correlation between objective and perceived pathogen risk have been addressed using ecologically valid measures in a global sample. The current article reports two studies addressing these gaps. In Study 1, we include a global sample (n = 361) and tested the influence of both perceived pathogen exposure and an objective measure of pathogen risk-local communicable infectious disease mortality rates-on individual differences in pathogen and sexual disgust sensitivities. In Study 2, we first replicate Study 1's analyses in another large sample (n = 821), targeting four countries (US, Italy, Brazil, and India); we then replaced objective and perceived pathogen risk with variables specific to the SARS-CoV-2 pandemic. In Study 1, both local infection mortality rates and perceived infection exposure predicted unique variance in pathogen and sexual disgust. In Study 2, we found that perceived infection exposure positively predicted sexual disgust, as predicted. When substituting perceived and objective SARS-CoV-2 risk in our models, perceived risk of contracting SARS-CoV-2 positively predicted pathogen and sexual disgust, and state case rates negatively predicted pathogen disgust. Further, in both studies, objective measures of risk (i.e., local infection mortality and SARS-CoV-2 rates) positively correlated with subjective measures of risk (i.e., perceived infection exposure and perceived SARS-CoV-2 risk). Ultimately, these results provide two pieces of foundational evidence for the behavioral immune system: 1) perceptions of pathogen risk accurately assay local, objective mortality risk across countries, and 2) both perceived and objective pathogen risk explain variance in disgust levels.

Project description:Robustness and plasticity are essential features that allow biological systems to cope with complex and variable environments. In a constant environment, robustness, i.e., insensitivity of phenotypes, is expected to increase, whereas plasticity, i.e., the changeability of phenotypes, tends to diminish. Under a variable environment, existence of plasticity will be relevant. The robustness and plasticity, on the other hand, are related to phenotypic variances. As phenotypic variances decrease with the increase in robustness to perturbations, they are expected to decrease through the evolution. However, in nature, phenotypic fluctuation is preserved to a certain degree. One possible cause for this is environmental variation, where one of the most important "environmental" factors will be inter-species interactions. As a first step toward investigating phenotypic fluctuation in response to an inter-species interaction, we present the study of a simple two-species system that comprises hosts and parasites. Hosts are expected to evolve to achieve a phenotype that optimizes fitness. Then, the robustness of the corresponding phenotype will be increased by reducing phenotypic fluctuations. Conversely, plasticity tends to evolve to avoid certain phenotypes that are attacked by parasites. By using a dynamic model of gene expression for the host, we investigate the evolution of the genotype-phenotype map and of phenotypic variances. If the host-parasite interaction is weak, the fittest phenotype of the host evolves to reduce phenotypic variances. In contrast, if there exists a sufficient degree of interaction, the phenotypic variances of hosts increase to escape parasite attacks. For the latter case, we found two strategies: if the noise in the stochastic gene expression is below a certain threshold, the phenotypic variance increases via genetic diversification, whereas above this threshold, it is increased mediated by noise-induced phenotypic fluctuation. We examine how the increase in the phenotypic variances caused by parasite interactions influences the growth rate of a single host, and observed a trade-off between the two. Our results help elucidate the roles played by noise and genetic mutations in the evolution of phenotypic fluctuation and robustness in response to host-parasite interactions.

Dataset Information

Pathogen evolution under host avoidance plasticity.

Publications

Pathogen evolution under host avoidance plasticity.

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