Recently introduced inter-specific Musa hybrids, bred for improved yield and resistance to diseases, have been found to be widely infected with several Banana streak badnavirus (BSV-Obino I'Ewai (BSV-OI), BSV-Imové (BSV-Im) and BSV-GoId Finger (BSV-Gf) strains), the causal agent of banana streak disease (BSD). One hypothesis suggests that BSD occurrence in these inter-specific hybrids results from activation of corresponding BSV endogenous pararetrovirus sequences (EPRVs) integrated into the Musa genome rather than from external sources of infection. The process of genetic hybridisation and abiotic stress such as micropropagation by in vitro culture may be responsible in triggering episomal expression of these BSV integrants. In order to test the first hypothesis we carried out a genetic analysis of banana streak disease incidence in a F1 triploid (AAB) population produced by hybridisation between virus- and disease-free M. balbisiana Pisang Klutug Wulung PKW (BB diploid) and M. acuminata IDN 110T (AAAA tetraploid) parents. Molecular AFLP markers segregating with the presence or absence of episomal viral particles were identified in the M. balbisiana genome only. These data indicate that a genetic mechanism is involved in BSV appearance, and suggest that a monogenic allelic system confers the role of carrier to the M. balbisiana parent The three different strains were detected by IC-PCR in diseased hybrids. The BSV-OI and BSV-Im strains appeared in almost all diseased hybrids while the BSV-Gf strain appeared only in about half of these hybrids. Genetic analysis resulting from AFLP results showed that BSV-OI EPRVs' regulation depends on a genetic factor: BEL (BSV Expressed Locus) (Lheureux et al. 2003). Further experiments showed that BSV-lm EPRVs' regulation depends on the same genetic factor too. Even if BSV-Gf appears only in half of diseased hybrids, some elements suggest that BSV-Gf strain appearance and the activation of its corresponding EPRV(s) se