Banana streak viruses (BSV) infect bananas and plantains worldwide. They are naturally transmitted by mealybugs; however infections can also occur in the absence of vectormediated transmission, through the activation of infectious endogenous BSV sequences (eBSVs). Infectious eBSVs are present in the genome of Musa balbisiana spp, which are important progenitors for breeding improved banana varieties. Once activated by biotic or abiotic stresses, these viral sequences cause spontaneous infection in both natural and synthetic interspecific hybrids harbouring the M. balbisiana genome, denoted B [1]. Therefore, the presence of infectious eBSVs within B genomes is currently the main constraint for breeding banana and plantain interspecific hybrids and for exchanging Musa germplasm. The sequence and organization of eBSVs in the diploid M. balbisiana genitor Pisang Klutuk Wulung (PKW) was elucidated [2], showing that integration of infectious eBSGFV [3] and eBSOLV is di-allelic, with one infectious and one non-infectious allele, whereas that of infectious eBSImV is monoallelic [2]. Taking advantage of the development of allele-specific molecular markers [2; 4], eBSV signatures were established for all M. balbisiana genitors of the CIRAD Guadeloupe Musa collection. This work unveiled important differences between accessions. All combinations of infectious and non-infectious alleles were observed for the three BSV species, as well as complete and uncomplete integrants when compared to those described in PKW. Breeding improved M. balbisiana progenitors devoid of infectious eBSGFV and/or eBSOLV alleles was undertaken through self-pollination and chromosome doubling of haploid lines. Both approaches successfully lead to M. balbisiana cultivars devoid of infectious eBSOLV and/or eBSGFV resulting from the segregation of eBSOLV and eBSGFV alleles. Improved lines of one particular M. balbisiana cultivar, cv. Honduras, originally free of eBSImV, were shown to be free of infectious e