The segment UTRs are known to contain signals for transcription, replication and packaging of vRNP [24, 27, 28, 30] . We now show that the identity of the 39 and 59 UTRs also influences the competition between different segments. Relatively minor differences were observed when reporter genome segments with different natural UTRs were compared in the competition assay. This result is in agreement with the observation that non- conserved regions of the UTRs contribute to some but limited extent to viral RNA replication [28, 31] . However, introducing three nucleotide changes in the 39 UTR (G3A/U5C/C8U) of the NP segment, which is predicted to stabilize the UTR panhandle structure and is known to lead to increased reporter gene expression in infected cells [23] , dramatically increased the competitive ability of the reporter segment, both when replication/transcription was driven by transfection of polymerase-and NP-encoding segments and when mediated by IAV infection. Thus, while reporter segments carrying the natural NP UTRs or the mutant NPph UTRs were both efficiently expressed in the absence of competitor segments, large differences in luciferase expression were observed in favor of the luciferase segment carrying the panhandle-stabilizing mutations when other reporter segments were co-transfected or in IAV infected cells. In agreement herewith, recombinant viruses carrying two nucleotide changes (G3A/C8U) in the UTR of either the PB1 or PA segment displayed enhanced replication/transcription of the mutated segments in detriment of the wild-type UTR-bearing segments [32] .