In addition to being susceptible to infection by bacterial and fungal pathogens, Drosophila is also a natural host for viruses such as Drosophila C virus (DCV), Drosophila X virus (DCX) and Flock House virus, and, perhaps surprisingly, by a broad variety of viruses causing disease in humans such as Sindbis virus, vesicular stomatitis virus (VSV; a virus of the Rhabdoviridae family, which includes the well-known rabies virus), Rift Valley fever virus, dengue virus and West Nile virus (Cherry et al., 2005; Cherry et al., 2006; Cherry and Perrimon, 2004; Galiana-Arnoux et al., 2006; van Rij et al., 2006; Wang et al., 2006) . Genome-wide RNAi screens have identified several important host factors that are exploited by viruses, such as factors required selectively for replication of influenza virus (Hao et al., 2008) or propagation of dengue virus (Sessions et al., 2009) . Similarly, viruses such as DCV that have transcripts with internal ribosome-binding sites depend on several host translation factors that are not required for other types of viruses lacking these sites (Cherry et al., 2005) . DCV also requires the host factor COPI to generate a vesicular compartment, which is necessary for viral replication, and COPI is also required for the replication of the related poliovirus in human cells (Cherry et al., 2006) . As another example, infection by vaccinia virus (the prototypical poxvirus) was found to depend on the AMP-activated kinase (AMPK) complex, the master energy sensor of the cell, for endocytic entry and actin remodeling (Moser et al., 2010) . The authors found a similar requirement for AMPK in facilitating vaccinia infection of mouse embryonic fibroblasts and showed that this kinase was also involved in viral entry via the process of macropinocytosis.