Mechanisms of Toxoplasma gondii persistence and latency

William Sullivan, Victoria Jeffers

Research output: Contribution to journalArticle

109 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)717-733
Number of pages17
JournalFEMS Microbiology Reviews
Volume36
Issue number3
DOIs
StatePublished - May 2012

Fingerprint

Toxoplasma
Parasites
Cysts
Toxoplasmosis
Immunity
Gene Expression

Keywords

  • Apicomplexa
  • Differentiation
  • Eukaryotic pathogen
  • Microbial persistence
  • Parasite
  • Stress response

ASJC Scopus subject areas

  • Microbiology
  • Infectious Diseases

Cite this

Mechanisms of Toxoplasma gondii persistence and latency. / Sullivan, William; Jeffers, Victoria.

In: FEMS Microbiology Reviews, Vol. 36, No. 3, 05.2012, p. 717-733.

Research output: Contribution to journalArticle

Sullivan, William ; Jeffers, Victoria. / Mechanisms of Toxoplasma gondii persistence and latency. In: FEMS Microbiology Reviews. 2012 ; Vol. 36, No. 3. pp. 717-733.
@article{c488a0b2a18c459e9aa75f1c3326f8f1,
title = "Mechanisms of Toxoplasma gondii persistence and latency",
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.",
keywords = "Apicomplexa, Differentiation, Eukaryotic pathogen, Microbial persistence, Parasite, Stress response",
author = "William Sullivan and Victoria Jeffers",
year = "2012",
month = "5",
doi = "10.1111/j.1574-6976.2011.00305.x",
language = "English",
volume = "36",
pages = "717--733",
journal = "FEMS Microbiology Reviews",
issn = "0168-6445",
publisher = "Wiley-Blackwell",
number = "3",

}

TY - JOUR

T1 - Mechanisms of Toxoplasma gondii persistence and latency

AU - Sullivan, William

AU - Jeffers, Victoria

PY - 2012/5

Y1 - 2012/5

N2 - 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.

AB - 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.

KW - Apicomplexa

KW - Differentiation

KW - Eukaryotic pathogen

KW - Microbial persistence

KW - Parasite

KW - Stress response

UR - http://www.scopus.com/inward/record.url?scp=84859350581&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84859350581&partnerID=8YFLogxK

U2 - 10.1111/j.1574-6976.2011.00305.x

DO - 10.1111/j.1574-6976.2011.00305.x

M3 - Article

C2 - 22091606

AN - SCOPUS:84859350581

VL - 36

SP - 717

EP - 733

JO - FEMS Microbiology Reviews

JF - FEMS Microbiology Reviews

SN - 0168-6445

IS - 3

ER -