Print PageResearch based on the study of infectious diseases has emerged as a mature program in both ecology and evolutionary biology. However, ecological and evolutionary theories for infectious diseases remain largely independent of each other. Ecological theory of infectious diseases is dominated by mathematical approaches utilizing systems of differential equations to describe the changes in the susceptible and infectious portions of a host population. Expansions and expositions of this approach have led to a deeper understanding of the ecological processes that govern the initiation, spread and persistence of infectious diseases. The evolutionary study of infectious diseases includes analyses developed in the tradition of population genetics, including recent techniques based in coalescent theory, as well as revealing the fitness tradeoffs that shape the evolution of virulence, antimicrobial resistance, host switching, and the coevolution of pathogen and their hosts. Reciprocal interactions between ecological and evolutionary processes governing a population are, however, expected to be commonplace and theoretical structures that simultaneously treat ecological and evolutionary dynamics will add significantly to our understanding of disease emergence and spread.
Results/Conclusions
We present a new approach for revealing the ecological processes that govern the spread of disease by uncovering currently underutilized patterns present within a viral phylogeny. Our approach combines several measures of phylogenetic structure with a computational model that simulates epidemiological dynamics and the concurrent molecular evolution of the pathogen. We view the structure of a phylogeny in terms of the topology of branches and nodes that define the hierarchical relationship between nucleotide sequences and the scaling of the topology in time and space. The measures we apply capture different aspects of phylogenetic structure, including the temporal pattern of branching and the relationship between sequence and geographic distance, and reveal the changes produced under the action of different ecological processes. We apply our approach to revealing the genomic and phylogenetic signatures produced by long distance translocation (LDT) of the host. We parameterize our model to reflect the ecology and evolution of the raccoon rabies epidemic that has spread through the eastern United States (US) from 1975 to the present. We find that there are several linearizable relationships between the rate of host movement and our measures of phylogenetic structure. Our approach can increase the degree to which we are able to resolve the details of a unobserved historical epidemic spread of a disease from sequence data derived from contemporary viral sequence data
