A major challenge in infectious disease control is the high degree of genetic diversity exhibited by many pathogens and their hosts. Understanding how this diversity emerged, how it is naturally structured and how it may be altered by public health interventions is of obvious value to the epidemiologist, but is also fascinating from an ecological and evolutionary perspective.
Several successful human pathogens exhibit antigenic diversity, as a means of camouflaging themselves from their host’s immune response. Differences amongst hosts, or between different tissues in the same host, can drive structural diversity in pathogen receptor binding molecules, as well as metabolic diversity in pathogen housekeeping genes.
For the host’s part, diversity is seen in the genes of the immune system, particularly in those responsible for pathogen recognition (e.g. the human leukocyte antigens). Physiological variation can can also play a role in determining the outcome of infection: the sickle cell mutation in haemoglobin is a well-known example, providing over 90% protection against death from malaria.
The interactive evolution of these various elements of pathogen and host diversity is central to our research. We develop and test mathematical models to understand these processes in many different disease systems including malaria, influenza, HIV and range of bacterial diseases.
Genome-wide transposon mutagenesis indicates that Mycobacterium marinum customizes its virulence mechanisms for survival and replication in different hosts.
Comparative multi-locus phylogeography of two Palaearctic spruce bark beetles: influence of contrasting ecological strategies on genetic variation.