Evolutionary models often pre-suppose the existence of constraints that limit realizable combinations of organismal traits. These constraints may be life-history trade-offs or bounds to trait evolution. Together, they imply that organisms are constrained to evolve within some region or domain in trait space. A classic example of a life-history tradeoff is the transmission-virulence tradeoff among pathogens which presumes that there is a positive relationship between transmission rate and virulence. The transmission-virulence trade-off has been used to explain why pathogens often kill/injure their hosts, instead of evolving to the epidemiological optimal combination of traits in the absence of such trade-offs, i.e., a benign pathogen with high transmission and low virulence. Although such trade-offs, and other bounds on trait evolution, are thought to emerge from lower-level constraints (e.g. molecular, biophysical, immunological or developmental), rarely can such constraints be predicted from first principles. Recent work on the biophysical and gene regulatory basis of the exploitation of bacteria by bacterial viruses suggests an opportunity to link molecular processes to the unfolding of phage life-history evolution.

Results/Conclusions

In this talk, we will discuss two efforts to model the molecular basis of life-history constraints in bacterial viruses (aka phages) and how they impact evolution of traits: (i) the probability of entering latency as a function of viral multiplicity of infection; (ii) the relationship between mortality of and burst size in virulent phages. In the first case, the choice between alternative cell fates is known to occur in phages and in other viruses. The choice between lysis and latency among phages emerges from the dynamics of a gene regulatory switch – a switch which depends sensitively on the number of co-infecting viruses. The dependence of switch dynamics on viral densities provides a mechanism for exploring how the evolution of latency is constrained by kinetic parameters of binding related to viral gene regulation. In the second case, we will discuss recent work on a mechanistic-based life history trade-off between mortality and reproduction among phages. In both cases we apply evolutionary models to assess how ecological dynamics arise from and are modified by regulatory and biophysical information. We will show how traits can evolve in these multi-scale models, as well as discuss how molecular-based constraints impact the long-term evolution of distinct phage strains.