Why is living fast dangerous? Disentangling the roles of resistance and tolerance of disease

Background/Question/Methods

Primary host developmental tempo axes (HDT; e.g., large-small body size continuum, slow-quick return continuum) represent a latent biological process and are increasingly used to predict which hosts contribute disproportionately more to pathogen transmission (competence). HDT’s influence on competence depends on how HDT influences host resistance and tolerance of disease. Here, we use structural equation modeling methodology to address known limitations of conventional measures of HDT, resistance, and tolerance. We first review conventional measures of HDT, resistance, and tolerance. We then provide a general ‘resistance-tolerance’ structural equation meta-model, from which system specific models can be derived. Finally, we derive a model specific to a group of generalist, vectored viruses that infect hundreds of grass species worldwide. We tested the model using experimental inoculation data for six phylogenetically paired grass species.

Results/Conclusions

Our review of conventional HDT, resistance, and tolerance measures revealed that they do not clearly map to theory. Analysis of our greenhouse experiment with structural equation models showed that 1) host traits covaried according to a prominent HDT axis, the slow-quick continuum; 2) the slow-quick continuum’s total effect was an increased impact of infection on biomass and resistance explained >78 percent of the slow-quick continuum’s total effect; and 3) phylogenetic control was necessary to measure the slow-quick return continuum, resistance, and tolerance. This study provides a framework for modeling HDT and its influence on epidemiological parameters. Moreover, it provides further evidence that HDT’s main influence on host competence is via resistance.