The role of GPI-linked surface proteins in site-specific tropism of Eimeria parasites and the potential of these proteins for novel therapies

Lead Research Organisation: The Pirbright Institute
Department Name: UNLISTED

Abstract

Eimeria parasites cause severe enteritis (coccidiosis) in chickens and remain a major welfare and economic problem. There are seven speces that infect chickens and each one of these grows in a different region of the gut. Following infection, chickens develop natural immunity to the infecting species of Eimeria, but remain fully susceptible to infection with the other six species. We have been carrying out detailed analysis of the GPI-linked surface antigens (SAGs) of Eimeria tenella. These are variant antigens that are expressed from two large multi-gene families located in four clusters within the E. tenella genome. We have found that SAGs are strictly developmentally regulated in their expression and that the dominant sporozoite SAG (EtSAG1) is not expressed in later merozoite stages, whereas many other SAGs are expressed solely by these later parasites. We have also shown that SAGs have adhesive properties, suggesting a role for them in binding to host cells. Recently we carried out some preliminary work on the SAGs of other species of Eimeria and found that they too have multiple SAG genes that are distantly related to, but quite distinct from, those of E. tenella. Given that SAGs are constitutively expressed on the surface of the parasite, they are ideally placed to interact with the host and therefore be important determinants of site specificity. They are also likely to be strong inducers of anti-parasite immunity. In this proposal we will: (1) determine if GPI-linked surface antigens (SAGs) of Eimeria play a role in the exquisite site specificity displayed by different species (E. tenella and E. maxima) that infect the chick; (2) elucidate whether developmental expression of EtSAG1 is a mechanism to optimise survival of the later stages of the parasite in the face of host immunity; (3) determine whether developmentally regulated SAGs can be targeted for the development of novel prophylactics against coccidiosis.

Publications

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