Mathematical models have been successfully applied previously to characterize the in vivo virus replication kinetics of HIV [31, 32] , hepatitis B and C [33, 49] , and influenza [34, 36, 50] , as well as in vitro viral yield experiments studying the effects of antiviral drugs [35] and the optimization of vaccine production [51, 52] . Models of viral plaques have also been considered [53] [54] [55] , although these were primarily directed at phage growth in an agar suspension of bacteria, a slightly different system than the cell monolayers considered here.