Growth of gene-rearranged viruses. We also employed our model to predict the growth of VSV strains having the N gene first position on the genome grows best, followed by N2, N3, and N4. This result is consistent with the previously suggested hypothesis that relocation of the N gene to 39-distal positions on the genome would be an efficient way to attenuate VSV for vaccine use [20] . The reduction in growth that follows from moving the N gene likely reflects, at least in part, an imbalance between replication and transcription. Insufficient production of N protein would reduce the extent of encapsidation of nascent anti-genome and thereby allow transcription to dominate over genome replication [41] . While the simulation matches the growth ranking, it did not quantitatively match the experimental data. The predicted variation in virion production (N1 ! N4: 4.7-fold decrease) is smaller than the experimentally observed variation (N1 ! N4: 16.7-fold decrease). A potential source of this quantitative difference was our neglect of mass action effects of N proteins on the encapsidation process in our model; encapsidation was simulated as an instantaneous process when free N proteins were available. As shown above, our model could capture the major effects of gene rearrangement on viral growth and protein expression.