Primary axes of host developmental tempo (HDT; e.g., large-small body size continuum; slow-quick return leaf continuum) represent latent biological processes and are increasingly used to a priori identify hosts that contribute disproportionately more to pathogen transmission. HDT's influence on host contributions to transmission depends on how HDT influences both resistance and tolerance of disease. Here, we use structural equation modeling to address known limitations of conventional measures of resistance and tolerance. We first provide a general 'resistance-tolerance' meta-model, from which system-specific models can be derived. We then develop a model specific to a group of vector-transmitted viruses that infect hundreds of grass species worldwide. We tested the model using experimental inoculations of six phylogenetically paired grass species. We found 1) host traits covaried according to a prominent HDT axis, the slow-quick continuum; 2) infection caused a greater reduction in the performance of quick-returns and >80 percent of that greater impact was explained by lesser resistance; 3) no resistance-tolerance tradeoff; and 4) phylogenetic control was necessary to measure the slow-quick continuum, resistance, and tolerance. These results support the conclusion that HDT's main influence on host contributions to transmission is via resistance. More broadly, this study provides a framework for quantifying Hit's influence on host contributions to transmission.