Greg Dwyer, Ph.D. Associate Professor Department of Ecology & Evolution Committee on Evolutionary Biology Biological Sciences Collegiate Division Office: Erman 102A | Phone: (773) 834-7691 | Fax: (773) 702-9740 | email:gdwyer(at)uchicago(dot)edu Subjects: Host-pathogen, spatial ecology, mathematical modelling, mathematical biology, population ecology, population dynamics, disease ecology, disease resistance, gypsy moth, polyhedrosis virus, baculovirus

Research Interests

Ecology and Evolution of Infectious Disease

Research in my lab is focused on the ecology and evolution of infectious diseases, and especially on how mathematical models can help us understand disease dynamics. The main diseases that we work on are baculoviruses, fatal, directly transmitted pathogens of forest insects. Through our work on baculoviruses, we have developed extensive expertise in statistical methods of fitting epidemic models to data, and this has led to more recent work on using models to understand epidemics in human populations. Finally, our interest in host-pathogen coevolution has led to work on using host-pathogen models to explain the maintenance of disease resistance genes in the model plant Arabidopsis thaliana.

Gypsy Moth larva eating oak leaf

Insect Pathogens

Many forest insects undergo dramatic boom-bust population fluctuations known as outbreaks, and baculoviruses play a key role in driving these fluctuations. Because baculoviruses are species-specific, and because they cause massive mortality in insect populations, there is a strong potential for coevolution between insects and baculoviruses. Much of our work has therefore aimed at understanding the role of host-pathogen coevolution in insect outbreaks. Forest insects also interact strongly with their host plants and with generalist predators and so we also study the effects on outbreaks of interactions between multiple species.

To understand coevolution and insect outbreaks, we use a combination of mathematical models, field experiments, and molecular-genetic tools. The models that we use relate the dynamics of baculovirus epidemics within host generations to the long-term dynamics of outbreaks. Our work has shown that a combination of baculovirus pathogens and generalist predators causes insect outbreaks to occur at highly irregular intervals. These irregular fluctuations are due to “stochastic chaos”, in which a small amount of randomness sustains chaos-like behavior in a system that might otherwise be stable.

NPV Polyhedra

To understand the role that coevolution plays in outbreaks, we have quantified the transmission of a nucleopolyhedrovirus, a baculovirus that attacks gypsy moths. Our experiments have shown that heterogeneity in susceptibility among gypsy moth larvae is so high that it leads to unrealistic stable behavior in the models, unless we also allow for evolutionary changes in resistance. Our experiments have further shown that host resistance is heritable, and that it fluctuates because of fluctuating selection, rising after outbreaks because of high disease mortality, and declining after outbreaks because of a cost or resistance.

To understand the mechanisms determining host resistance, we have recently begun to disentangle the components of transmission. Baculoviruses are transmitted when larvae accidentally consume leaves contaminated with other virus-killed larvae, and so both the feeding behavior of larvae and the chemical composition of foliage can affect transmission. In fact, gypsy moth larvae are known to avoid virus-contaminated foliage, and we have shown that this behavior is heritable. We are therefore extending our models to allow for this behavior, by constructing individual-based models that relate host behavior to the dynamics of epidemics. We have also shown that fluctuations in tannins, defensive compounds of the oaks that gypsy moths feed on, can modulate transmission, and our modeling work has shown that fluctuations in these compounds may play a key role in insect outbreaks. A major challenge is then to integrate these different influences on disease transmission into a coherent picture of pathogen-driven outbreaks.

In studying the transmission of the gypsy moth virus, we have come to realize that viruses differ substantially in their virulence, as measured by speed of kill. Because this difference is clearly heritable, we are beginning a sequencing project to identify loci that determine variability in virulence. Because the viral genome is only 162 kb, we can easily sequence hundreds of virus strains at once. Using our library of several hundred natural isolates of the gypsy moth virus, we can then use high-throughput sequencing to construct a SNP map of the viral genome. We will then genotype each of our isolates at each locus of interest. Because we know the outbreak dynamics at each site from which we collected each isolate, we will then be in a position to relate sequence variability to host-pathogen dynamics.

Finally, over the last 20 years, North American gypsy moth populations have also been attacked by the fungal pathogen Entomophaga maimaiga. This disease differs from the baculovirus in being strongly affected by weather conditions, including both moisture and temperature. We are therefore extending our insect host-pathogen models to allow for multiple pathogens, and especially to consider the effects of stochasticity in transmission.

Human Pathogens

A key part of our work with insect pathogens has been the development of methods of fitting models to data. This work has shown that understanding disease dynamics requires that we use mathematical models to combine data on epidemics with data on the effects of disease in individuals. Most models of human pathogens, however include vast numbers of parameters, without considering how the cumulative variability in these parameters might affect the reliability of model predictions. By using Bayesian statistical techniques, we have shown that the total uncertainty in the predictions of smallpox bioterrorism models is vast, and that this uncertainty has important implications for public-health strategies.

Our current work in this area is in collaboration with Vanja Dukic of the Department of Health Studies, and Ken Alexander of the Department of Pediatric Infectious Diseases. We are attempting to understand the effects of vaccination strategies on the dynamics of human papillomavirus, or HPV. HPV is a sexually transmitted disease that is the causative agent of cervical cancer, and leads to cancers in males as well. An effective HPV vaccine has recently been developed, and so we are developing mathematical models to evaluate different vaccination strategies.

Plant Pathogens

Our work with host-pathogen interactions has also branched out to consider plant pathogens, in collaboration with Joy Bergelson of the Department of Ecology and Evolution. We are exploring the extent to which the ecology of the interaction between the host plant and its pathogens is reflected in patterns of variability in DNA sequence data. In particular, we are using game-theoretic models to understand how host variability in resistance is maintained over the long term. By adapting the models to allow for both mutation and genetic drift, we can directly compare the model predictions to sequence data from host resistance genes. Our results suggest that host-pathogen models can play a key role in understanding the evolution of resistance genes, and imply that complex dynamics of allele frequencies play a major role in maintaining genetic variability.

Recent Publications

Abbott, K. C. and G. Dwyer. 2008. Using mechanistic models to understand synchrony in forest insect populations: the North American gypsy moth as a case study. The American Naturalist, in press.

Elderd, B., J. Dushoff, and G. Dwyer. 2008. Does Natural Selection on Disease Susceptibility Play a Role in Insect Outbreaks? The American Naturalist, in press.

Abbott K. C. and G. Dwyer. 2007. Food limitation and insect outbreaks: complex dynamics in plant-herbivore models. Journal of Animal Ecology 76:1004-1014.

Drury, K. L. S., Drake J. M., Lodge D. M., Dwyer G. 2007. Immigration events dispersed in space and time: factors affecting invasion success. Ecological Modelling. 206:63-78.

B. Elderd, V. Dukic, and G. Dwyer. 2006. Uncertainty in predictions of disease spread and public-health responses to bioterrorism and emerging diseases. Proceedings of the National Academy of Sciences. 103 (42): 15693-15697.

L. Crozier, and G. Dwyer. 2006. Combining population-dynamic and ecophysiological models to predict climate-induced insect range shifts. The American Naturalist. 167: 853-866.

J. Drake, J., K. L. S. Drury1, D. M. Lodge, A. Blukacz, N.D. Yan and G. Dwyer. 2006. How Many Animals Does it Take to Cause an Invasion? Demographic Stochasticity, Environmental Variability, and Windows of Invasion Risk for Bythotrephes longimanus in North America. Biological Invasions. 8:843-861.

G. Dwyer and W. F. Morris. 2006. Resource-dependent dispersal and the speed of biological invasions. The American Naturalist. 167 (2): 165-176.

K. L. S. Drury and G. Dwyer. 2005. Combining stochastic models with experiments to understand the dynamics of monarch butterfly colonization. The American Naturalist. 166: 731-750.

V. D’Amico, J. S. Elkinton, J. P. Buonaccorsi, and G. Dwyer. 2005. Pathogen clumping: an explanation for non-linear transmission of an insect virus. Ecological Entomology. 30: 383-390.

G. Dwyer, J. Firestone, and T. E. Stevens. 2005. Should models of disease dynamics in insect herbivores include the effects of variability in host-plant foliage quality? The American Naturalist. 165:16-31.

G. Dwyer, J. Dushoff, and S. Harrell Yee. 2004. The combined effects of pathogens and predators on insect outbreaks. Nature. 430:341-345. (This article was featured in Nature’s News and Views section: L. Stone. 2004. Population ecology: A three-player solution. Nature. 430:299-300.)

J. Dushoff and G. Dwyer. 2001. Evaluating the risks of engineered viruses: Modeling pathogen competition. Ecological Applications. 11 (6): 1602-1609.

J. Bergelson, G. Dwyer, and J.J. Emerson. 2001. Models and data on plant-enemy coevolution. Annual Review of Genetics. Vol. 35: 469-499.

Perry, W.L., J.L. Feder, G. Dwyer, and D.M. Lodge. 2001. Hybrid zone dynamics and species replacement between Orconectes crayfishes in a northern Wisconsin lake. Evolution. 55 (6): 1153-1166.

G. Dwyer, J. Dushoff, J.S. Elkinton, and S.A. Levin. 2000. Pathogen-driven insect outbreaks revisited: building models from experimental data. The American Naturalist, 156 (2): 105-120.

E.A. Stahl, G. Dwyer, R. Mauricio, M. Kreitman, and J. Bergelson. 1999. Dynamics of disease resistance polymorphism at the Rpm1 locus of Arabidopsis. Nature 400: 667-671.

A.F. Hunter and G. Dwyer. 1999. Insect population explosions synthesized and dissected. Integrative Biology. 1(5):166-177.

G. Dwyer, J.S. Elkinton , and A.E. Hajek. 1998. Spatial scale and the spread of a fungal pathogen of gypsy moth. The American Naturalist. 152: 485-494.

V. D'Amico, J.S. Elkinton, G. Dwyer, R.B. Willis, and M.E. Montgomery. 1998. Foliage damage does not affect within-season transmission of an insect virus. Ecology. 79: 1104-1110.

G. Dwyer, J.S. Elkinton, and J.P. Buonaccorsi. 1997. Host heterogeneity in susceptibility and the dynamics of infectious disease: tests of a mathematical model. The American Naturalist. 150: 685-707. (This paper received the Mercer Award of the Ecological Society of America).

W.F. Morris and G. Dwyer. 1997. Population consequences of constitutive and inducible plant resistance: herbivore spatial spread. The American Naturalist. 149: 1071-1090.

V. D'Amico, J.S. Elkinton, G. Dwyer, and J.P. Burand. 1996. Virus transmission in gypsy moths is not a simple mass-action process. Ecology, 76: 201-206.

J. S. Elkinton, G. Dwyer, and A. Sharov. 1995. Modelling the epizootiology of gypsy moth nuclear polyhedrosis virus. Computers and Electronics in Agriculture. 13:91-102.

G. Dwyer and J. S. Elkinton. 1995. Host dispersal and the spatial spread of insect pathogens. Ecology, 76:1262-1275.

Dwyer, G. 1994. Density-dependence and spatial-structure in the dynamics of insect pathogens. The American Naturalist. 143:533-562.

Dwyer, G. and J.S. Elkinton. 1993. Journal of Animal Ecology. Using simple models to predict virus epizootics in gypsy-moth populations.

Dwyer, G. 1992. On the spatial spread of insect pathogens: theory and experiment. Ecology 73:479-494.

Dwyer, G. 1991. The roles of density, stage and patchiness in the transmission of an insect virus. Ecology 72(2):559-574.

Dwyer, G., S.A. Levin, and L. Buttel. 1990. A simulation model of the population dynamics and evolution of myxomatosis. Ecological Monographs. 60:423-447.