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Our objective is to determine the mechanism by which Perkinsus marinus acquires iron from its host and how available iron controls the gene expression in the parasite, particularly in those aspects related to its proliferation and intracellular survival. Free or protein-bound iron is an essential factor for many apicomplexan parasites and for most eukaryotic cells in culture. P. marinus proliferation rates in vitro are highly dependent on available iron. The degree of concentration of metals such as iron, in the oyster host Crassostrea virginica is related to environmental factors. It is possible that, in the case of P. marinus and C. virginica, we are either witnessing the early stages of host/parasite co-evolution or a recent imbalance in a system that was stable prior to the l950s when mass mortalities became apparent. ln order to understand the cause(s) of oyster mortality we need to establish not only the source of P. marinus virulence and the oyster's apparent lack of effectiveness in countering these virulence factors, but also the environmental variables that influence both processes. Our research program is directed at understanding the host-parasite interaction that exists between the eastern oyster Crassostrea virginica and the protozoan parasite Perkinsus marinus ("Dermo") by identifying genetic and molecular events that are critical for P. marinus' host specificity, hemocyte entry, intracellular survival and proliferation. Our previous work has: demonstrated the inhibitory effect of iron chelators on P. marinus' growth rates; demonstrated an increase of growth rates in the presence of exogenous glycoproteins; and established a fully defined medium for P. marinus culture. We will focus on determining the molecular adaptations P. marinus utilizes to avoid intracellular destruction within the hemocytes of its host and the specific role of iron availability in determining intracellular survival.