Abstract

Purpose of Review

Despite over a third of the world’s population being chronically infected with Toxoplasma gondii, little is known about this largely asymptomatic phase of infection. This stage is mediated in vivo by bradyzoites within tissue cysts. The absence of overt symptoms has been attributed to the dormancy of bradyzoites. In this review, we reexamine the conventional view of chronic toxoplasmosis in light of emerging evidence challenging both the nature of dormancy and the consequences of infection in the CNS.

Recent Findings

New and emerging data reveal a previously unrecognized level of physiological and replicative capacity of bradyzoites within tissue cysts. These findings have emerged in the context of a reexamination of the chronic infection in the brain that correlates with changes in neuronal architecture, neurochemistry, and behavior that suggest that the chronic infection is not without consequence.

Summary

The emerging data driven by the development of new approaches to study the progression of chronic toxoplasma infection reveals significant physiological and replicative capacity for what has been viewed as a dormant state. The emergence of bradyzoite and tissue cyst biology from what was viewed as a physiological “black box” offers exciting new areas for investigation with direct implications on the approaches to drug development targeting this drug-refractory state. In addition, new insights from studies on the neurobiology on chronic infection reveal a complex and dynamic interplay between the parasite, brain microenvironment, and the immune response that results in the detente that promotes the life-long persistence of the parasite in the host.

Document Type

Article

Publication Date

12-2016

Notes/Citation Information

Published in Current Clinical Microbiology Reports, v. 3, issue 4, p. 175-185.

© Springer International Publishing AG 2016

The copyright holder has granted the permission for posting the article here.

This is a post-peer-review, pre-copyedit version of an article published in Current Clinical Microbiology Reports. The final authenticated version is available online at: https://doi.org/10.1007/s40588-016-0045-3.

Digital Object Identifier (DOI)

https://doi.org/10.1007/s40588-016-0045-3

Funding Information

Preparation of this article was supported in part by NIH/NIAID R21AI122894 awarded to APS and IDeA award from NIH/NIGMS 5P30GM110787 (COBRE for the Center for Molecular Medicine. PI Louis B Hersh, University of Kentucky) project awarded jointly to APS and MSG.

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