Inter-specific Musa hybrids have been found to be infected with Banana streak pararetrovirus Obino I'Ewai strain (BSV-Ol) responsible of Banana Streak Disease (BSD). One hypothesis suggest (i) that BSD occurrence in these hybrids results from activation of BSV-Ol endogenous pararetrovirus sequences (EPRVs) integrated into the Musa genome rather than from external sources of infection and (ii) that the process of genetic hybridisation may be one factor involved in triggering episomal expression of the BSV integrants. In order to test this hypothesis we carried out a genetic analysis of BSD incidence in a F1 triploid (AAB) population produced by hybridisation between virus- and disease-free M. balbisiana (BB) and M. acuminata (AAAA) parents. Half of the F1 progeny expressed BSV particles. Ten AFLP markers co-segregating with the absence and/or presence of BSV infection were identified in the M. balbisiana genome only. Analysis of the segregation of these markers allowed the construction of a genetic map containing the focus associated with BSV infection called BSV Express Locus (BEL). A genetic mechanism is involved in BSV appearance, conferring the role of carrier to the M. balbisiana parent. Two previously unidentified BSV strains in addition to BSV-Ol, have been furthermore detected in these diseased hybrids: BSV-Imové (BSV-Im) and BSV-Gold Finger (BSV-GF) strains. The BSV-Ol and BSV-Im strains appeared in almost all diseased hybrids while the BSV-GF strain appeared only in about half of these hybrids. The close relationships between the presence of these two new BSV strains and the presence of corresponding EPRVs in the M. balbisiana parent genome shows that the M. balbisiana genome contains at least two other pathogenic BSV EPRVs: BSV-Im and BSV-GF EPRVs. Genetic analysis resulting from AFLP results showed that BSV-0l and BSV-Im EPRVs' expression depends on the same genetic factor, the BEL locus. Although the BSV-GF is not genetically linked to th