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Infect. Immun. doi:10.1128/IAI.00085-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Toxoplasma gondii strains lacking oral transmission are defective in stage differentiation

Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO 63110, USA.; Department of Microbiology, University of Tennessee, Knoxville, TN, 37996

^* To whom correspondence should be addressed. Email: sibley{at}borcim.wustl.edu.

	Abstract

Toxoplasma gondii undergoes differentiation from rapidly growing tachyzoites to slowly growing bradyzoites during its life cycle in the intermediate host, and conversion can be induced in vitro by stress. Representative strains of the three clonal lineages showed equal capacity to differentiate into bradyzoites in vitro as evidenced by induction of BAG1, staining with the lectin Dolichos biflorus (DBL), pepsin resistance, and oral infectivity to mice. We also examined several recently described exotic strains of T. gondii, which are genetically diverse and have a different ancestry from the clonal lineages. The exotic strain COUG was essentially like the clonal lineages and showed a high capacity to induce bradyzoites in vitro and in vivo, consistent with its ability to be efficiently transmitted by the oral route. In contrast, exotic strains MAS and FOU, which are defective in oral transmission, showed a decreased potential to develop into bradyzoites in vitro. This defect was evident by reduced staining with the lectin DBL and the cyst antigen CST1, failure down-regulate tachyzoite antigens such as SAG1 and SAG2A, and decreased resistance to pepsin treatment. Despite normal in vitro differentiation, the exotic strains CAST and GPHT also showed decreased oral transmission due to formation of smaller cysts and a lower tissue burden during chronic infection, traits also shared by MAS and FOU. Collectively, these findings reveal that limited oral transmission in some strains of T. gondii is due to inefficient differentiation to the bradyzoite form, leading to defects in formation of tissue cysts.

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