Theoretical studies have explored varying evolutionary relationships between heightened virulence and extreme pathogen longevity [4,5,12,17,18,19]. One critical component of these studies revolves around whether virulence evolves independently of free-living survival. For example, some models have argued [4] that pathogen virulence is independent of survival under a set of conditions: when the host–pathogen system is at an equilibrium (evolutionary and ecological), if host density fluctuates around an equilibrium, or if turnover of the infected host population is fast relative to the pathogen in the environment. However, if the host–pathogen system is at disequilibrium and if the dynamics of propagules in the environment are fast compared to the dynamics of infected hosts, then virulence is, as hypothesized, an increasing function of propagule survival [4]. Kamo and Boots [17] examined this hypothesis by incorporating a spatial structure in the environment using a cellular, automata model and found that, if virulence evolution is independent of transmission, then long-lived infective stages select for higher virulence. However, if there is a tradeoff between virulence and transmission, there is no evidence for the Curse of the Pharaoh hypothesis, and in fact, higher virulence may be selected for by shorter rather than long-lived infectious stages. Further, the evolution of high virulence does not have to occur solely through a transmission–virulence tradeoff. Day [18] demonstrated how pathogens can evolve high virulence and even select for traits to kill the host (e.g., toxins) if pathogen transmission and reproductive success are decoupled. These studies emphasized the context-dependence of virulence–survival relationships. Understanding where in the relationship between virulence and survival a given pathogen population exists may allow one to understand how virus evolution will manifest at the level of epidemics.