The emergence of new viral diseases typically occurs when a strain acquires a mutation that allows it to infect a new host species. This extremely important epidemiological problem can be better understood through the lens of ecological and evolutionary theory. For this talk we will explore how ecological niche theory and evolutionary theory on historical contingency and adaptation can inform the processes that lead to host-range expansions. Our discussion will be of results from a model viral system studied in the lab; phage λ and its host bacterium Escherichia coli. Through a combination of viral genomics and experimental evolution approaches we have reconstructed the ecological conditions and evolutionary events essential for the virus to evolve to infect new species of bacteria.

Results/Conclusions

By allowing a number of replicate E. coli and phage λ communities to coevolve, we found that some of the viral populations evolved to target a new receptor (OmpF) that the ancestor was unable to exploit. This new function has the side-effect of allowing the virus to infect completely new genera of bacteria (e.g. Klebsiella). Only populations in a particular resource environment evolved the new function, and of all of those, only 25 out of 95 replicate communities evolved it. The environmental specificity of this adaptation combined with its rarity suggests that its evolution occurs as a complex interplay between ecology, chance mutation, and co-evolution. We found that a sequence of three events is required: First, the bacteria must evolve resistance by mutations in a regulatory gene (malT) of the phage receptor (lamB), which only occur in certain environments. Second and third, the phage counters with two successive mutations in its gene for the protein used for bacterial recognition (Jgp). This study provides an example of the complex and stochastic steps required for an organism to gain a key innovation, as well as a systematic example of how a virus can expand its host-range.