Based on previous findings of Cav-1 involvement in the late retroviral life cycle [13] we investigated the influence [20] . This question may be answered in a Cav-1 (-/-) MDCK cell line, which yet has to be established. Data from knock-down experiments in MDCK were supplemented by transfection of a dominant-negative Cav-1 mutant as well as Cav-1 over-expression, which decreased viral yields by 38-44%. The results are reminiscent of experiments of Nystrom et al. who observed impairment of the insulin signalling pathway upon expression of both, the dominant-negative Cav-1 mutant and the over-expressed Cav-1 wt cDNA as well [21] . Finally, competition with M2 fusion proteins impaired virus replication, too.