Mechanisms of Toxoplasma gondii persistence and latency

Authors

  • William J. Sullivan Jr,

    Corresponding author
    1. Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA
    • Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA
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  • Victoria Jeffers

    1. Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, IN, USA
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Correspondence: William J. Sullivan Jr, Department of Pharmacology and Toxicology, Indiana University School of Medicine, 635 Barnhill Drive, MS A-525, Indianapolis, IN 46202, USA. Tel./fax: 317 274 1573/7714; e-mail: wjsulliv@iupui.edu

Abstract

Toxoplasma gondii is an obligate intracellular protozoan parasite that causes opportunistic disease, particularly in immunocompromised individuals. Central to its transmission and pathogenesis is the ability of the proliferative stage (tachyzoite) to convert into latent tissue cysts (bradyzoites). Encystment allows Toxoplasma to persist in the host and affords the parasite a unique opportunity to spread to new hosts without proceeding through its sexual stage, which is restricted to felids. Bradyzoite tissue cysts can cause reactivated toxoplasmosis if host immunity becomes impaired. A greater understanding of the molecular mechanisms orchestrating bradyzoite development is needed to better manage the disease. Here, we will review key studies that have contributed to our knowledge about this persistent form of the parasite and how to study it, with a focus on how cellular stress can signal for the reprogramming of gene expression needed during bradyzoite development.

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