Abstract
Once the acute phase of Toxoplasma gondii infection resolves, the parasite remains latent as bradyzoite forms that persist within tissue cysts. The stress-induced conversion of tachyzoites to bradyzoites is a critical step in pathogenesis of toxoplasmosis, because latent bradyzoite forms can reactivate with waning immune function and are infectious to other hosts. Despite their biological importance, the biology of bradyzoites and the molecular mechanisms for developmental transition are not well understood. Bradyzoites express unique antigens and metabolic enzymes and are encased within a highly glycosylated cyst wall, This chapter reviews our progress in understanding unique structural components of bradyzoite cysts and the signalling processes that lead to T. gondii persistence.
Original language | English (US) |
---|---|
Title of host publication | Toxoplasma Gondii |
Subtitle of host publication | The Model Apicomplexan - Perspectives and Methods: Second Edition |
Publisher | Elsevier Ltd. |
Pages | 521-549 |
Number of pages | 29 |
ISBN (Print) | 9780123964816 |
DOIs | |
State | Published - Sep 2013 |
Keywords
- Bradyzoite
- Cyclic AMP
- Cyst
- Differentiation
- Glycosylation
- Heat shock proteins
- Latency
- Parasitophorous vacuole
- Stress
ASJC Scopus subject areas
- Immunology and Microbiology(all)