Mechanisms of Toxoplasma gondii persistence and latency.

Mechanisms of Toxoplasma gondii persistence and latency.
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DOI:
10.1111/j.1574-6976.2011.00305.x
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发表时间:
2012-05
影响因子:
11.3
通讯作者:
Jeffers V
Jeffers V
中科院分区:
生物学1区
文献类型:
--
作者:
Sullivan WJ Jr;Jeffers V

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刚地弓形虫是一种专性细胞内原生动物寄生虫,可引起机会性疾病,特别是在免疫功能低下的个体中。其传播和发病机制的核心是增殖阶段(速殖子)转化为潜伏组织囊肿(慢殖子)的能力。包囊使弓形虫能够在宿主体内持续存在,并为寄生虫提供了一个独特的机会,可以在不经过性阶段的情况下传播到新的宿主身上,而性阶段仅限于猫科动物。如果宿主免疫力受损,慢殖子组织囊肿可引起重新激活的弓形虫病。为了更好地控制这种疾病,需要更好地了解协调慢殖子发育的分子机制。在这里,我们将回顾一些重要的研究,这些研究有助于我们了解这种寄生虫的持久形式以及如何研究它,重点是细胞应激如何为慢殖子发育过程中所需的基因表达重编程发出信号。
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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