We used MDCK (ATCC CCL-34), a canine kidney cell line commonly used in basic influenza virus research and vaccine production [16] [17] [18] [19] . To elucidate the biological importance of Cav-1 in the influenza life cycle, MDCK cells were infected with a selectable retroviral Cav-1 RNAi vector carrying a puromycin-resistance gene (RVH1-Puro-Cav-1) as well as control RVH1-Puro alone [20] . We found that the Cav-1 content decreased gradually to 25% of the value in wild-type MDCK at 14 1, 1, 10) . Notably, the experiments revealed similar results with an average decrease of influenza titres to 57.3% of wild-type levels ( Fig. 1) . The statistical analysis of nine independent experiments revealed that the 1.5-3 fold reduction in titres observed is highly significant (paired t-test, >99% confidence, p > 0,01) When cells stably transduced with control virus vector devoid of Cav-1 interfering sequences (RVH1puro) were infected with influenza A virus (m.o.i. = 10) titres of released virus was affected only marginally. Thus, we conclude that Cav-1 reduction in MDCK is correlated with a decrease in influenza virus progeny. This suggests, that Cav-1 directly or indirectly affects the human influenza virus life cycle in MDCK cells.