Mechanisms of Toxoplasma gondii persistence and latency

dc.contributor.authorSullivan, William J., Jr.
dc.contributor.authorJeffers, Victoria
dc.contributor.departmentPharmacology and Toxicology, School of Medicine
dc.date.accessioned2024-08-29T08:20:33Z
dc.date.available2024-08-29T08:20:33Z
dc.date.issued2012
dc.description.abstractToxoplasma 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.
dc.eprint.versionAuthor's manuscript
dc.identifier.citationSullivan WJ Jr, Jeffers V. Mechanisms of Toxoplasma gondii persistence and latency. FEMS Microbiol Rev. 2012;36(3):717-733. doi:10.1111/j.1574-6976.2011.00305.x
dc.identifier.urihttps://hdl.handle.net/1805/43018
dc.language.isoen_US
dc.publisherOxford University Press
dc.relation.isversionof10.1111/j.1574-6976.2011.00305.x
dc.relation.journalFEMS Microbiology Reviews
dc.rightsPublisher Policy
dc.sourcePMC
dc.subjectParasite
dc.subjectApicomplexa
dc.subjectDifferentiation
dc.subjectEukaryotic pathogen
dc.subjectMicrobial persistence
dc.subjectStress response
dc.titleMechanisms of Toxoplasma gondii persistence and latency
dc.typeArticle
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