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Cell Mol Life Sci. 2018 Jul;75(13):2355-2373. doi: 10.1007/s00018-018-2808-x. Epub 2018 Mar 30.

A latent ability to persist: differentiation in Toxoplasma gondii.

Author information

1
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. jeffersv@iu.edu.
2
Departments of Medicine, Microbiology and Immunology, and Pathology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
3
Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, FL, 33612, USA.
4
Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
5
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.

Abstract

A critical factor in the transmission and pathogenesis of Toxoplasma gondii is the ability to convert from an acute disease-causing, proliferative stage (tachyzoite), to a chronic, dormant stage (bradyzoite). The conversion of the tachyzoite-containing parasitophorous vacuole membrane into the less permeable bradyzoite cyst wall allows the parasite to persist for years within the host to maximize transmissibility to both primary (felids) and secondary (virtually all other warm-blooded vertebrates) hosts. This review presents our current understanding of the latent stage, including the factors that are important in bradyzoite induction and maintenance. Also discussed are the recent studies that have begun to unravel the mechanisms behind stage switching.

KEYWORDS:

Bradyzoite; Differentiation; Encystation; Epigenetics; Gene regulation; Immunity; Latency; Tachyzoite; Toxoplasma; Toxoplasmosis

PMID:
29602951
PMCID:
PMC5988958
DOI:
10.1007/s00018-018-2808-x
[Indexed for MEDLINE]
Free PMC Article

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