The goals of this project are to (i) break the cycle of schistosomiasis transmission in endemic areas, and (ii) contribute to the wider understanding of
a) mechanisms used by molluscs to attack and kill parasites, andRecent data have appreciably deepened our understanding of the mechanisms responsible for the resistant host phenotype in the Biomphalaria glabrata-Schistosoma mansoni PR-1 strain host-parasite model (Bayne CJ, Hahn UK and Bender RC (2001) Mechanisms of molluscan host resistance and parasite escapes. Parasitology 123. Supplement: Flukes and Snails Revisited, edited by D. Rollinson; co-ordinating editor L.H. Chappell. S159 – S167).
Our aims now are to experimentally verify or reject new hypotheses so as to be able to describe events at the molecular level in both compatible and incompatible host-parasite combinations. Our rationale is that transmission of schistosomiasis to mammalian hosts depends on the outcomes of encounters between this parasite and its intermediate host, and that interruption of the intra-molluscan phase of the life cycle therefore provides a means of stopping transmission.
Our studies will yield a fuller understanding of the genetic basis of susceptibility and resistance in the host and of infectivity in the parasite in trematode-mollusc parasitism.
Our overarching hypothesis is this: in the early stages of molluscan schistosomiasis, products of the host hemocyte respiratory burst and oxyradical scavenging counter-defenses of the parasite are major determinants of the parasite’s fate, while additional factors also influence outcomes.
In the course of pursuing these goals with methods that include proteomic analyses, we anticipate obtaining novel DNA sequences for B. glabrata, and these will be made available through this web site and GenBank
- This project is funded by NIH through August 2006.