One parameter, the infectious lifespan of a cell, t I , had very little effect on either the plaque velocity or the viral titer growth rate. In the latter case, this parameter was explicitly neglected in the derivation of the growth rate, because earlier viral yield experiments have shown little cell death prior to the peak of the virus concentration (see, e.g., [38, 39] ). The fact that, over a wide range of infectious lifespan values, the resulting plaque velocity remained unchanged, is perhaps more surprising. Indeed, a shorter infectious lifespan will lead to the earlier appearance of plaques, resulting in larger plaque sizes at any given time. We have shown, however, in earlier work where influenza virus plaques were observed by immunostaining [41] , that the same plaque velocity can be measured from both the progress of dead cells, as we consider here, and the progress of newly infected cells. This indicates that plaque velocity is established at the advancing edge of an infection wave, and is likely unaffected by cell death in the wake of that wave. In those experiments, the infectious lifespan of a cell appears only as a time-delay between the infected cell plaque growth and the dead cell plaque growth. This has also been observed for the plaques of other viruses [42] . Since the infectious lifespan has little effect on the experiments we consider, and is therefore not identifiable here, we have fixed its value for both strains and for all simulations to value of t I~1 2h, obtained from the literature ( Table 1) .