Epidemics are dynamical processes with variable rates of disease progress. How much of these changes in disease rate are triggered by the host population is still a pending issue. An epidemic is driven by its effective reproduction number: the product between the proportion of susceptible tissue, the rate of disease transmission, and the duration of the infectious period. Then, any modification in the host population, either quantitative or qualitative (distribution of plants or of susceptible organs) may have an impact on the epidemic dynamics. The growth of the host population is modified by architectural features or by cultural or agronomical practices. The production of new organs continuously modifies the porosity of the plant or of the canopy and its level of susceptibility if organ susceptibility changes with age (ontogenic resistance). Indirectly, plant growth modifies the micro-climatic environment inside the canopy, generating favourable or unfavourable conditions for pathogens. The organ susceptibility, or their susceptibility period, may also be modified by cultural practices disrupting the crop-pathogen synchronisation. These variations within host populations do impact disease incidence, severity or spread. However, they have rarely been explicitly taken into account in epidemiological models. Tracking back from the global dynamics of an epidemic the pathogen processes that are impacted and ranking the host traits involved in their modifications represents a challenge. In this paper, we will 1) review evidence of epidemic variations attributed to plant growth and architecture in main pathosystems, 2) list the pathogen processes impacted, and give some clue to identify and assess them in different epidemic contexts and 3) explore models able to measure and predict the effect of plant growth and architecture on epidemics.Read less <