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Infection and Immunity, September 2009, p. 3731-3739, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00450-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

A Transmembrane Domain-Containing Surface Protein from Toxoplasma gondii Augments Replication in Activated Immune Cells and Establishment of a Chronic Infection{triangledown}

Angela M. Pollard, Sini Skariah,{dagger} Dana G. Mordue,{dagger} and Laura J. Knoll*

Department of Medical Microbiology and Immunology, University of Wisconsin—Madison, Madison, Wisconsin 53706

Received 22 April 2009/ Returned for modification 29 May 2009/ Accepted 26 June 2009

Toxoplasma gondii mutants identified as defective in the establishment of chronic infection were screened to isolate those specifically impaired in their ability to replicate within activated macrophages. One of the identified mutants contains an insertion in the hypothetical gene TGME49_111670. Genetic complementation restores the ability of the mutant to replicate in immune cells and produce cysts in the brains of mice. While the mutant is more sensitive to nitric oxide than is its parental strain, it is not defective in its ability to suppress nitric oxide. The disrupted protein has no significant homology to proteins with known functions, but is predicted to have one transmembrane domain. Immunofluorescence shows the protein on the parasite surface, even in activated macrophages, colocalizing with a tachyzoite surface antigen, SAG1, and oriented with its C-terminal end external. Western analysis reveals that the protein is downregulated in bradyzoites. Despite the tachyzoite specificity of this protein, mice infected with the mutant succumb to acute infection similarly to those infected with the parent strain. Serum samples from mice with chronic T. gondii infection react to a polypeptide from TGME49_11670, indicating that the protein is seen by the immune system during infection. This study is the first to characterize a T. gondii surface protein that contains a transmembrane domain and show that the protein contributes to parasite replication in activated immune cells and the establishment of chronic infection.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of Wisconsin—Madison, 1550 Linden Drive, Madison, WI 53706. Phone: (608) 262-3161. Fax: (608) 262-8418. E-mail: ljknoll{at}wisc.edu

{triangledown} Published ahead of print on 6 July 2009.

Editor: J. F. Urban, Jr.

{dagger} Present address: Department of Microbiology and Immunology, New York Medical College, Valhalla, NY 10595.

Infection and Immunity, September 2009, p. 3731-3739, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00450-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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