Through modeling and simulation of two common in vitro experiments, the plaque and viral yield assays, we have extracted We have shown that seemingly contradictory results from the two experiments -plaques of the susceptible strain grow more quickly than the resistant strain, while the reverse is true of their titer growth in viral yield assays -can be considered complementary views of the infection kinetics which allow for the determination of parameter values controlling the replication of each strain. Specifically, we have found that the latent infection period of the H275Y mutant strain -equal to the time elapsed between the successful infection of a cell by a virion and the significant release of virus progeny by the newly infected cell -is much longer than that of the WT strain (by 4-10 h). The infectivity of the mutant strain, however, was found to be much higher than the WT, as quantified by the infecting time -equal to the time for a single infectious cell to cause the latent infection of one other, within a completely susceptible cell population. Independent single-cycle viral yield assay results lend support to the hypothesis of a longer latent infection period for the mutant strain than the WT, but suggest a more moderate (*2h) difference between the two. These results are consistent with the larger NA activity of the susceptible (WT) strain compared to the H275Y mutant, reported here and by others [25] , and its increased NA surface expression [24] . Since neuraminidase is the viral surface enzyme responsible for cleaving the virus from its sialic-acid receptors at the cell surface [47] , it can be expected that an increase of its expression would lead to more rapid viral release (a shorter latent infection period for the WT strain) but may also hinder the subsequent attachment of virions to other cells, leading to decreased infectivity (longer infecting times).