Genetic Diversity and Disease - A Progress Report on the Rust, the Smut, and Other Problematic Parasites
Does genetic diversity limit the spread of infectious diseases? We would likely answer "yes" if we looked at the history of intensive agriculture. Time and time again, disease epidemics have decimated dense stands of genetically homogenous crops. That coffee you might be drinking right now doesn't come from Sri Lanka, once a major region for coffee production: the industry collapsed when a rust fungus swept through the vast monocultures of coffee trees on the island in the late 1800's. Stories like this made it almost common knowledge that there is a "monoculture effect:" infection transmits readily between genetically similar individuals, so we expect higher infection prevalence in genetically homogenous populations. But agricultural systems are unique - they're far denser and far less diverse than most wild populations. Outside of agriculture, controlled experiments of the relationship between disease and diversity have produced mixed results. Does genetic diversity generally limit the spread of infectious diseases, across a range of systems, and, if so, how strong is the effect? Answering this question requires a quantitative synthesis of the results of multiple independent experiments. I'll tell you about my current endeavors to address this need. I'll also discuss my attempt to test the old, but somewhat neglected, idea that low diversity populations should have higher variance in infection prevalence than high diversity populations.
I'd also like to flip this question around - what about the parasites? Is genetic diversity important for them? Theory would say 'yes, it's very important!' A major evolutionary hypothesis argues that sexual reproduction should be more common in parasitic species than in their free-living relatives. The idea here is that sexual parasites can produce genetically diverse offspring, and these are, on average, more likely to succeed at infecting a host population that is constantly counter-adapting. There's some data to support this idea - sexual outcrossing is quite common in parasites, even when it seems terribly inconvenient. Some asexual parasites, however, are very successful, with broad geographic and/or host ranges. Why do asexual parasites succeed in some places/hosts and not others? Are there meaningful patterns across taxa? More generally, does any of the progress we've made on the problem of sex help us understand the biogeographic distribution of sex in nature? In the second part of the talk, I'd like to present these conceptual issues that I'm working to review.