The Evolutionary ecology of physiological constraints in ecological communities and HPV-induced cancer
thesisposted on 13.12.2012, 00:00 authored by Paul A. Orlando
I use consumer resource theory and evolutionary game theory in developing theory with regards to physiology, protists, and viruses. I use differential equation consumer resource systems to provide an ecological basis for theoretical exploration. And I use game theory to model natural selection within an ecological context. I investigate the effects of stoichiometric constraints on consumers in a graphical framework. I found that when stoichiometry is integrated into consumer resource models, ecological communities take on a more complex array of possible states. When resource equilibrium abundances are low, ecological communities are nearly identical to those used to characterize animal communities based on substitutable resources. However, when resource equilibrium abundances are high, ecological communities are similar to those used to characterize plant communities based on essential resources. I investigate the effects of species that can switch trophic levels by a morphologic transformation on ecological communities. I found that these species often stabilize population dynamics, which favors each morph as a separate species. I conclude that switching species likely evolve in environments with stochastic resource fluctuations or extrinsic drivers of resource levels. I also found that although switching species can fill diverse ecological niches in a community, they do not necessarily restrict diversity. I investigate the role of digestive physiology coupled with the digestive properties of resources in structuring ecological communities. I found that bulky resources select for large guts with long throughput times, and high energy/volume resources select for small guts and short throughput times. Most resource pairs lead to the evolution of a specialist on the richer resource followed by the invasion and evolution of a generalist. I also applied theory to HPV induced cancers. I hypothesized that HPV faces a life history tradeoff, where HR HPV is persistent but not very infectious, and vice versa for low-risk HPV. We found that different sexual subcultures within the human population could explain the origin and maintenance of these distinct HPV types. Furthermore, I made a PDE model of HPV infection within mucosal tissue to discover the links between cell population dynamics and HPV protein expression. And how somatic evolution of cells produces tissue level changes. I found that HPV’s proteins likely increase the density of tissue at which cells can divide and possibly also slow the migration rate of cells to the skin surface. I also found that somatic evolution is an alternative explanation for tissue level changes observed during high-risk HPV infection.