The appearance of the aggressive bird influenza (H5N1), the 2009 outbreak of a pandemic influenza (H1N1) of swine influenza origin, and the recent occurrence and rapid dissemination of oseltamivir-resistant human influenza strains are motors that have accelerated the search for new antiviral targets and agents within the last time [37] [38] [39] . The investigation of cellular mechanisms involved in 'early' and 'late' viral processes and the identification of cellular actors provides a means to interfere with viral strategies. With this respect, the observed Cav-1/M2 interplay may represent a new, conserved target for e.g. therapeutic intervention with circulating and newly emerging strains of human influenza A virus. Thus, appli-cation of high-throughput screening of compound libraries will follow target identification and may result in a new antiviral agent, as exemplified for a cellular target involved in the late retroviral life cycle [40] . When this manuscript was in preparation Zhou et al. reported binding of a cytoplasmic fragment of M2 from human influenza to Cav-1 in an in vitro assay based on a Cav-1 protein fragment expressed in E. coli and CBDdependent perinuclear co-localization upon expression in CHO cells [41] . However, no experiments on the functional importance of M2/Cav-1 were performed in this investigation.