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 (<em>Ne</em>) 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 <em>Ne</em> 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 <em>Ne</em> at the inoculation step, (ii) understand the mechanisms used by the plant to control <em>Ne</em> 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 <em>Capsicum annuum</em>. 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.< Réduire