Like the mRNAs of the host cell, influenza virus mRNAs are capped and polyadenylated (reviewed in Neumann, 2004). The methylated caps, however, are scavenged from host cell mRNAs and serve as primers for viral RNA synthesis, a process termed 'cap-snatching' (Krug, 1981; Hagen, 1994). The PB2 polymerase protein binds the cap, activating endonucleolytic cleavage of the host mRNA by PB1. The 3' poly-A tracts on viral messages are generated by polymerase stuttering on poly-U tracts near the 5' end of the template vRNA (Robertson, 1981; Zheng, 1999). The second process allows polyadenylation of viral mRNAs when the host cell polyadenylation process has been inhibited (Engelhardt, 2006; Amorim, 2006). Notably, early transcripts (including NP and NS1) accumulate in the cytoplasm before late transcripts (M1, HA, and NS2), and in varying abundances, suggesting additional control mechanisms regulating viral gene expression (Shapiro, 1987; Hatada, 1989; Amorim, 2006).