To differentiate between those alternatives and identify the point of arrest in the viral life cycle induced by JMN3-003, we first examined whether the compound blocks membrane fusion and thus viral entry. Expression of plasmid-encoded paramyxovirus envelope glycoproteins in receptor-positive cells typically results in extensive cell-to-cell fusion, the hallmark cytopathic effect associated with most paramyxovirus infections in vitro [1] . Transient membrane fusion assays allow a quantitative assessment of whether an inhibitor blocks viral entry or post-entry steps of the viral life cycle [20, 34] . When we examined MeV glycoproteinmediated cell-to-cell fusion microscopically (figure 6A) and in a luciferase reporter-based quantitative cell-to-cell fusion assay (figure 6B) in the presence of JMN3-003, we observed extensive membrane fusion indistinguishable from that seen in vehicletreated controls, indicating that the compound does not act as an entry inhibitor.