Seeking a more detailed correlation between locations of the two genes and the viral phenotypes relevant to vaccine application, we simulated in silico the growth of all mutants that retain the gene order P -M -L of the wild-type, but allow G and N to move, criteria that define 20 possible geneorder permutations. The viral growth and the level of G protein in infected BHK cells mainly depend on the locations of N gene and G gene, respectively ( Figure 8A and 8B) , which is consistent with the experimental results of Flanagan et al. [39] . Further, if gene G is fixed, then moving gene N closer to the 39 promoter is predicted to increase protein G expression ( Figure 8B ). Consistent with this prediction, Flanagan et al. also observed a higher G protein expression for the G1N2 strain than for the G1N4 strain [39] . Enhanced replicative ability of VSV strain by locating its N gene at an earlier position in its genome can contribute to increasing the level of G protein. If either gene N or gene G is located at the fifth position, then both levels of virus growth and G protein expression are very low (Figure 8) , because with such genome organizations the stoichiometric amounts of N and G proteins required for replication and assembly (Table 2 , [28, 29] ) cannot be reached. Our simulations with the BHK cell parameters (Table 1 ) overall captured the experimentally established relative growth of the VSV strains in BHK-21 cells, but the growth of the G3N4 strain was significantly overestimated compared with the experimental results [39] ( Table 3 ). The relevant mechanism for such a large discrepancy between the simulation and the experimental results remains to be elucidated.