TY - JOUR T1 - Death of the assumption that ‘latent period’ is fixed over the course of a plant disease epidemic JF - bioRxiv DO - 10.1101/148619 SP - 148619 AU - Frédéric Suffert Y1 - 2017/01/01 UR - http://biorxiv.org/content/early/2017/06/16/148619.abstract N2 - The latent period is defined as the time between infection and the onset of sporulation due to that infection. It is a crucial life history trait, particularly for polycyclic plant diseases, because it determines how many complete infectious cycles can occur during an epidemic and its final intensity. Many studies have focused on the variation of latent period with pathogen or host genotype, or its plasticity in response to environmental factors. The focus on these aspects is unsurprising, as these factors classically form the apices of the epidemiological triangle (host, pathogen, and environment). Experiments in controlled conditions are generally used to assess pathogenicity (virulence and aggressiveness) and host susceptibility. Once estimated for one or several pairs of host-pathogen genotypes, the value of the parameter ‘latent period’ is implicitly considered to be fixed and is used “as is” in epidemiological models. Paradoxically, most epidemiological studies do not consider the latent period of a pathogen population to be variable. My thesis here is that the latent period can display non-negligible variability over the course of a disease epidemic, and that this variability has multiple sources, some of which have complex, antagonistic impacts. I develop arguments for four sources of variation challenging the implicit assumption that the latent period remains constant: daily fluctuations in leaf temperature, nature of the inoculum, host stage or age of host tissues, intra-population competition and selection for aggressiveness traits. I focus on the wheat fungal pathogen Septoria tritici blotch (Zymoseptoria tritici), making use of empirical datasets collected during my own research projects and a targeted literature review. Finally I discuss in which case certain sources of these variation should be accounted for into epidemiological models. ER -