Sarah Cobey


  • Assistant Professor, Department of Ecology and Evolution, & Committee on Microbiology


Postdoc, Harvard School of Public Health, 2010-2013
Ph.D, University of Michigan, 2009
A.B., Princeton University, 2002

Contact Information

The University of Chicago
205 Erman Hall
Chicago, IL 60637

Phone: (773) 795-0970


My research is concerned with the ecology and evolution of pathogens. I am interested in two main themes within this area: how ecological and evolutionary processes can influence each other, and how pathogens compete in the complex environment of the host immune system. 

The interaction of ecology and evolution in host-pathogen dynamics

The population dynamics of pathogens are often muddled by evolution, most obviously as a result of immune pressure from the host population but also potentially from the epidemic dynamics themselves. An interesting question is to what extent the evolutionary and epidemiological dynamics might feed back on one another, and with what effect. 

Influenza provides an exciting system for investigating this question. Previous work has suggested that chance discoveries of novel phenotypes by H3N2 result in dramatic shift in the genetic structure of the viral population and increase the prevalence of infections. Under what conditions do the epidemiological dynamics facilitate the creation or invasion of evolutionary novelty? Are these conditions under our control? A related puzzle is why the most fit strains of influenza tend to come from certain parts of the world. We are using computer simulations to test hypotheses that explain this pattern. From these insights, we can develop predictions for the evolution of influenza and other viruses. 

Pathogen competition under host immunity 

Host-pathogen interactions are complex consumer-resource dynamics. Not only do many pathogens evolve to escape host immunity, but each pathogen's phenotype also varies depending on which host is 'reading' it. This difference might arise, for example, from the host's particular immune history or chance. The potential for ambiguity in the pathogen's phenotype also depends on whether the pathogen triggers more of an innate or adaptive immune response. The breadth, strength, and specificity of immune pressure thus together shape the landscape in which pathogens interact. 

Work with collaborators has shown that differences in the strength and breadth of immunity can explain patterns of diversity in influenza and pneumococcus. How does immunity affect the structure of pathogen communities? Do common viruses and bacteria compete with or facilitate one another? We are developing statistical models to answer these questions. 

Broader themes 

I am interested in using host-pathogen systems as a lens to study basic themes in biology. How predictable is evolution, and can we anticipate when it will be constrained? How do niche and neutral processes contribute to patterns of pathogen diversity, and do their contributions shift over time? Is there evidence of evolved robustness in host microbial communities that share similar transmission routes? My long-term goal is to answer these and similar questions with models and data.

Selected Papers

Research Papers in PubMed