To further explore whether JMN3-003 meets the profile of a host-directed antiviral, we examined whether the extent of inhibition is determined by the species origin of the host cell used for virus propagation. Based on its broad host cell range, inhibition of influenza A/WSN replication was monitored. In addition to higher mammalian (HT1080 (ATCC CCL-121), HeLa (ATCC CCL-2), MDCK (ATCC CCL-34)) cell lines, cells of rodent (NIH-3T3 (ATCC CRL-1658), MEL B16 (ATCC CRL-6322), BHK-21 (ATCC CCL-10), CHO (ATCC CCL-61)) and avian (DF-1 (ATCC CRL-12203)) origin were tested, which are all permissive for influenza A/WSN infection (table 2) . While inhibitory concentrations obtained for all higher mammalian cell lines examined were similar, A/WSN inhibition by JMN3-003 was found inactive on some rodent cell lines and when virus was propagated on murine or avian cells (table 2) . However, inhibitory activity extended fully to primary human PBMCs (figure 2). For the latter, inhibition of MeV-Alaska was monitored due to efficient growth of MeV isolates on PBMCs [21] . The host cell species effect of antiviral activity of JMN3-003 is consistent with specific targeting of cellular factors by the compound, while arguing against docking to conserved viral factors or an undesirable promiscuous, unspecific mode of activity.