During the last decade the emergence of reverse genetics techniques has created unprecedented opportunities to better control viral attenuation [7] [8] [9] . Reverse genetics enables the production of RNA viruses from cloned cDNA, so specific mutations can be relatively easily introduced into viruses. The challenge to engineering viruses for attenuation then shifts from creating the variants to predicting how specific genetic changes define or correlate with measurable effects on virus growth. Such a challenge can be addressed through the development of quantitative and mechanistic models that map genome-level changes to the dynamics of virus growth under different environmental conditions. Models of intracellular virus growth aim to predict how rapidly a virus-infected cell will produce virus progeny. Inputs to such models include rates of constituent processes such as entry of the virus into the cell, transcription of viral mRNAs, translation of viral proteins, replication of viral genomes, assembly of intermediates, and finally, production and release of viral progeny. Decades of detailed biochemical, biophysical, and genetic studies have, for diverse viruses, contributed toward a level of mechanistic understanding of viral functions and interactions. Various intracellular models of virus growth have been developed for phage Qb [10] , phage T7 [11, 12] , HIV-1 [13] , and influenza A virus [14] .