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Infection and Immunity, January 2001, p. 501-507, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.501-507.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Initial Characterization of CST1, a Toxoplasma gondii Cyst Wall Glycoprotein

Yi Wei Zhang,1 Sandra K. Halonen,1,2 Yan Fen Ma,1 Murray Wittner,1 and Louis M. Weiss1,3,*

Department of Pathology, Division of Parasitology,1 and Department of Medicine, Division of Infectious Diseases,3 Albert Einstein College of Medicine, Bronx, New York 10461, and Department of Natural Sciences, Mercy College, Dobbs Ferry, New York 105222

Received 12 July 2000/Returned for modification 6 September 2000/Accepted 30 September 2000

Toxoplasma gondii is an important protozoan pathogen of humans that can cause encephalitis in immunocompromised individuals such as those with AIDS. This encephalitis is due to reactivation of latent infection in T. gondii-seropositive patients. Latent organisms survive within tissue cysts, which are specialized parasitophorous vacuoles containing bradyzoites. The cyst wall of this structure is produced by modification of the parasitophorous vacuole by the parasite and is important in cyst survival. The components of the cyst wall have been poorly characterized. By using immunofluorescence and immunoelectron microscopy, we have identified a monoclonal antibody (MAb 93.18) that reacts with the cyst wall. This antibody recognizes a 116-kDa glycoprotein, which we have termed CST1, containing sugar residues that bind Dolichos biflorans lectin (DBA). CST1 is distinct from T. gondii antigen labeled with succinyl Triticum vulgare lectin (S-WGA) and represents the major DBA-binding component in T. gondii. The carbohydrate components of the tissue cyst, such as CST1, are probably important in both providing stability and facilitating persistence in its host. As is seen in the carbohydrate capsules of fungi, glycoproteins in the T. gondii cyst wall may protect cysts from the immune response of the host. Further characterization of the formation of the cyst wall and its components should lead to insights into the mechanism of tissue cyst persistence and may suggest novel therapeutic approaches to eliminate tissue cysts of this organism.

* Corresponding author. Mailing address: Rm 504, Forchheimer Bldg., Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461. Phone: (718) 430-2142. Fax: (718) 430-8543. E-mail: lmweiss{at}aecom.yu.edu.

Infection and Immunity, January 2001, p. 501-507, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.501-507.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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