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Past Winner
2008 E.W.R. Steacie Memorial Fellowship

Troy Day

Mathematical Biology

Queen's University

Troy Day
Troy Day

The home page of Troy Day's Web site features a quote from ecologist Charles Elton that takes a pointed but humorous shot at mathematicians who entice biologists with stories of how much their research would benefit from a little immersion in mathematics, then toss them into the deep end with no life preserver. It's meant tongue in cheek, but underscores the fact that biologists don't always get along with math.

Dr. Day conquered that fear long ago, becoming convinced about the benefits of mathematical models while doing his master's degree in zoology. In fact, he thought highly enough of mathematics to choose it for his doctoral degree. These days he spends much of his time developing models for such things as the evolution of organisms that cause various diseases or the public health strategies used to control those diseases, work that has earned him a 2008 NSERC E.W.R. Steacie Memorial Fellowship.

In a world where travel makes it possible to transmit viruses or bacteria around the world in a matter of hours, the effectiveness of public health efforts depends on a good understanding of the life cycle of these pathogens as well as the mechanisms that make some of them deadly and others benign. That makes it possible to choose the best treatment or prevention options for individuals as well as the best public health strategies to limit the spread of disease.

For example, following the SARS outbreak in 2003, Dr. Day was able to demonstrate that the nature of the disease's life cycle meant that quarantining those suspected of contact actually did little to prevent infection, since they were not contagious until they had developed symptoms. While that lesson was learned after the fact, the analytical tools he developed can now be applied to any future disease outbreak.

Disease pathogens are a constantly moving target, however. Evolutionary pressures can change both their virulence and their life history. “There's sort of a race between driving something extinct and its ability to evolve away from the pressure you're imposing on it,” he says. “You're essentially creating a bad habitat for this thing and it will evolve to deal with that habitat. In an epidemiological context, you want to drive it extinct before it is able to do that.”

The failure to eradicate a pathogen can result in it becoming more virulent. Most people know that bacteria evolve resistance to antibiotics. Lesser known is the fact that virtually any human intervention can impact a species. Even vaccines, says Dr. Day, can exert an evolutionary influence.

Much depends on the type of organism, though. The measles virus seems to have little evolutionary capacity to avoid its vaccine. Influenza is quite another story, which means vaccines must continually be updated. “One of the interesting questions is what's different about those two viruses, and whether we can predict something about what we would expect to happen in other viruses,” he says.

“No matter what you do, you're going to introduce some novel selective pressure that will result in some kind of evolutionary change. Ideally, what you try to do is minimize the bad impacts of that.”

He plans to pursue this question further during his NSERC Steacie research. That includes trying to develop models that will predict the evolutionary consequences of pharmaceutical interventions, such as vaccines. He's collaborating with Andrew Read of the University of Edinburgh, a top expert in the experimental evolutionary epidemiology of malaria. While Dr. Read's lab conducts experiments on various components of the immune response in mice, Dr. Day's lab will use the data to develop and test his new theoretical approach. The goal is to develop a model that can be applied to diseases for which the in-host information is not available.

In developing these kinds of models, Dr. Day strives to balance the overall characteristics of a population with the behaviour of individual organisms. For example, in the case of the malaria parasite, he incorporates factors such as transmissibility and mortality, as well as the dynamics of how each parasite reproduces within a host.

Dr. Day says pathogens must strike a delicate balance in order to survive, and each one chooses a different path. Some reproduce very quickly, which increases the chances they'll get transmitted to another host, but threatens the host's survival. Others take a more laid back approach, doing relatively little harm to their host and buying themselves more time to transmit.

Learning more about each pathogen's preferences will lead not just to better choices in treatment and prevention, but can also help predict how emerging pathogens may behave. “Every disease is going to be different in terms of how these things work out. The challenge is to try to fit that into your predictive scheme in some way.”

In addition to receiving NSERC research grants for the past decade, Dr. Day also won an NSERC Doctoral Prize in 1999. When he's not using mathematics to do battle with microbes, he tries to help make the field more accessible to other biologists. He says his education and experience give him a good feeling for the most effective ways to broach the subject. In conjunction with The University of British Columbia biologist Sarah Otto, he's even written a book designed to help undergraduate students learn to stop worrying and love mathematics.