In banana (Musa sp.), two major species Musa acuminata (A genome) and Musa balbisiana (B genome) contribute to edible cultivars that are mostly triploids and highly sterile. The B genome contains, together with agronomical favorable traits, unwanted infectious endogenous viral integrations of Banana streak virus - (eBSV)-, responsible for the banana streak disease. We developed several PCR and Derived Cleaved Amplified Polymorphic Sequences (deCAPS) markers for genotyping eBSVs. Microsatellites markers (SSR) distributed all over chromosomes of the reference Musa sequence are also available. To understand the genetic regulation of infectious eBSV in the created interspecific hybrid, we monitored the distribution of infectious eBSVs among a F1 triploid (Musa AAB) population produced by hybridization between the tetraploid CRBP39 (AAAB) and the diploid M. acuminata (AA) Pahang. The CRBP39 is a plantain carrying both infectious eBSGFV and eBSOLV unlike Pahang, which is devoid of eBSV. Out of 195 offspring, 131 exhibit eBSGFV and eBSOLV, 41 have either eBSOLV or eBSGFV and 23 plants are lacking eBSV. This clearly indicates a strong bias in favor of progenies containing the B chromosome carrying eBSGFV and eBSOLV but also prove recombinations between M. balbisiana and M. acuminata genomes. To refine these analyses, the progeny is genotyped with a set of SSR covering the entire genome and covering more densely the B chromosome carrying eBSGFV and eBSOLV. The results will provide new information regarding chromosome pairing affinities between A and B Musa chromosomes. In addition, they will provide a description of the genetic makeup of each offspring to help understand the factors that facilitate the recovery of a functional viral genome from eBSV. (Texte intégral)