In compatible interactions between plants and viruses that result in systemic infection, symptom development is a major phenotypic trait. However, host determinants governing this trait are mostly unknown, and the mechanisms underlying it are still poorly understood. In a previous study on the Arabidopsis thaliana-Plum pox virus (PPV) pathosystem, we showed a large degree of variation in symptom development among susceptible accessions. Two basic types of interaction exist between a virus and its host plant: i) a compatible interaction associated with plant invasion and viral multiplication, followed in most cases by the induction of symptoms, and ii) an incompatible interaction with no or only limited viral multiplication or movement in the host plant. Plant-virus interactions are relatively well documented, but efforts have so far focused on resistance (or resistancebreaking) mechanisms and on the identification of their genetic determinants. Conversely, the one or more mechanisms controlling symptom development in plants are still largely unknown, so that only a very patchy picture of the interaction between a plant and a virus can be presented.