Infection of plants by viruses is a complex process that involves several steps: inoculation into plant cells, replication in inoculated cells, cell-to-cell movement during leaf colonization and long-distance movement during systemic infection. The success of the different steps is conditioned by the effective viral population size (Ne) defined as the number of individuals that pass their genes to the next generation. During the infection cycle, the virus population will endure several bottlenecks leading to drastic reductions in Ne and to the random loss of sorne virus variants. If strong enough, these bottlenecks could act against selection by eliminating the fittest variants. Therefore, a better understanding of how plant affects Ne rnay contribute to the developrnent of durable virus-resistant cultivars. We aimed to (i) identify plant genetic factors that control Ne at the inoculation step, (ii) understand the mechanisms used by the plant to control Ne and (iii) compare these genetic factors with other genes controlling virus life cycle and plant resistance durability. The virus effective population size was measured in a segregating population of 152 doubled-haploid lines of Capsicum annuum. Plants were inoculated mechanically either with a Patata virus Y (PVY) construct expressing the green fluorescent protein (OFP), or a necrotic variant of Cucumber mosaic virus (CMV), the CMV-N strain of Fulton. Ne was assessed by counting the number ofprimary infection foci observed on inoculated cotyledons under UV light for PVY -OFP or the number of necrotic local lesionsobserved on inoculated leaves for CMY-N. The numbers of primary infection foci and locallesions were correlated arnong the doubled-haploid lines (r=0.57) and showed a high heritability (h2=0.93 and 0.98 for PVY and CMV, respectively). The effective population size of the two viruses was shown to be controlled by botb common quantitative trait loci (QTLs) and virus-specifie QTLs, indicating the contribution ofboth general and specifie mechanisms. The PVY-specific QTL colocalizes with a QTL that had previously been shown to be involved in PVY accumulation and capacity to break amajor-effect resistance gene down.