The big questions…and how our lab is working to address them:

Are urban areas hotspots for disease evolution?

Our planet is increasingly urbanised, altering the evolution of organisms that live in cities and creating niches for pathogen emergence. Rodents and birds such as geese, gulls and sparrows are examples of urban-adapted organisms that we study due to their abundance and global distribution. Our lab is finding out how cities are changing the life history traits of these animals and whether this favors the evolution and transmission of pathogens. Current projects include testing whether cities are hotspots for avian influenza virus evolution in gulls across urban gradients in North America, evaluating the trade-off between lead contamination and adaptive immunity in house sparrows, and viral discovery using deep sequencing of the rat virome from populations that live among people who are houseless in urban Boston.


How is disease distribution changing due to the climate crisis?

High latitude ecosystems are expected to be increasingly disrupted by the climate crisis, with consequences for altering disease risk at the global scale. Our lab studies host-pathogen dynamics in the Arctic and sub-Arctic focusing on Alaska and Iceland to identify the evolutionary processes that shape viral fitness and how this is changing over time. We recently uncovered how morbilliviruses (such as Phocine Distemper Virus) have shifted to endemic circulation in seal populations that are rebounding from hunting pressure and are increasingly connected in the high Arctic. We also study source-sink dynamics of influenza A virus at high latitudes between North America and Eurasia and how rising sea surface temperatures are having a differential impact on the host ecology of wild birds and consequently disease epidemics.


Does domestication and trade of animals give rise to pathogens?

Microbes that we call ‚Äúpathogens” usually arise in the context of animal domestication or monocultures. In contrast, microbes that originate in wild animals rarely produce disease in their reservoir host. A prominent example is highly pathogenic avian influenza (HPAI) for which virulent strains evolve in poultry without going extinct due to the high density and turnover of birds. The process of domestication varies from country-to-country depending on geography, natural resources, local agricultural practices and the ecology of wildlife. Our lab studies the the evolution of pathogenicity at the wild-domestic interface and seeks to understand what molecular, organismal and ecological factors lead to virulence. This research occurs in partnership with collaborators in Bangladesh, Egypt and Zambia where we study the evolutionary pressures that increase disease risk along the food supply chain from subsistence farm to commercial market.


How dynamic is host immunity in space and time?

Immunity is not a static trait but is highly dynamic in space and time. Migratory animals provide a rich opportunity for elucidating trade-offs between immune function and energy expenditure caused by changes in life history. Our work on influenza A virus has shown that antibodies in wild birds accumulate with every migration cycle resulting in an antibody repertoire that expands over time. However, short-term declines in antibodies occurs when disease risk is low and energetic demands are high. We are investigating how the immune landscape changes in response to life-history, human pressures on the environment, and the emergence of novel strains to which there is minimal cross-reactive immunity. The extent to which immunity in reservoir hosts contributes to pathogen evolution is an important open question with implications for both animal and human health.