Of the strategies conceivable towards this goal, targeting host factors required for completion of the viral life cycle rather than pathogen-encoded factors directly has received heightened interest in recent years [14, 15] . This approach is expected to establish a significant barrier against spontaneous viral escape from inhibition, since individual viral mutations are less likely to compensate for the loss of an essential host cofactor than to prevent highaffinity binding of a conventional, pathogen-directed antiviral. Given some degree of overlap of host cell pathways required for successful replication of related viral pathogens, host-directed antiviral approaches also have the potential to move beyond the one-bug one-drug paradigm by broadening the pathogen target range of a chemical scaffold.