Dr. Sorensen's Research Projects
Variation in host life history patterns may be a result of a parasite adaptation, a host adaptation or a non-adaptive side effect of the interaction. Genetic heterogeneity of hosts and parasites fuels the coevolutionary arms race leading to an array of varied outcomes. In the coevolutionary interactions between participants, hosts respond to parasite selective pressures by evolving mechanisms for evading, counteracting, or minimizing the negative fitness effects of parasitism. We have suggested that a host may be able to modify the outcome of a parasitic infection either:
- by resisting infection via initiation of immune responses or
- by varying other life-history parameters.
The degree to which hosts exhibit these responses depends on numerous factors from the force of infection to the prevailing environmental conditions. The traditional view is that hosts prevent infection through genetically-based resistance to parasites. Resistance to infection is generally regarded as a costly undertaking that results in trade-offs with other life-history traits; however, empirical evidence for this view is lacking. One thrust of this laboratory is to assess the potential costs of resistance under varying biotic and abiotic conditions. Alternatively, hosts may alter infection outcomes by varying other (non-immunological) life-history characters, which may be less costly than resistance. Using the snail-trematode system as a model, we have been exploring the range of tactics utilized by molluscan hosts, including changes in reproductive output, survivorship, and growth. Overall, we hope to extend our view of parasite-induced host variation, address concepts of life history theory, and explore models that attempt to explain coevolutionary interactions between hosts and parasites.
Genetic Structure of Parasite Populations
Interactions between trematodes and their snail hosts play an important role in the development of the host and parasite genetic systems. The extent of genetic heterogeneity in local parasite populations has implications on the epidemiology of host disease. Blood flukes of the genus Schistosoma cause human schistosomiasis, a disease affecting more than 200 million patients worldwide. This parasite exhibits significant phenotypic differences within and among geographic populations, yet the degree of genetic variability in both the parasite and its host snails remains largely unknown. Heterogeneity of schistosome populations in nature is difficult to study due to the location of the adult worms within the human blood system and the small size of the larval stages that are associated with transmission of the parasite between hosts. We have been able to circumvent these difficulties by using single locus molecular probes (microsatellites) to quantify the degree of host and parasite genetic heterogeneity in natural populations and to determine how that variation changes on a spatial and temporal scale. We are assessing the genetic population structure of schistosome parasites from molluscan and human hosts in Brazilian villages utilizing molecular markers. In addition, both deterministic and simulation models are being developed to explore the role of genetic polymorphism in this host-parasite system. Results will yield evolutionary insights into the epidemiological process, help identify genetic consequences of control strategies, and complement concurrent immuno-epidemiology studies of humans in endemic Brazilian communities.