Understanding mechanisms and the role of differentiation in pathogenesis of Toxoplasma gondii: a review

Sullivan, William J.; Smith, Aaron T.; Joyce, Bradley R.

doi:10.1590/s0074-02762009000200005

Cited by 42 publications

(42 citation statements)

References 54 publications

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“…Transcriptional regulation clearly plays a major role in bradyzoite development as evidenced by numerous studies showing stage‐specific gene expression (Manger et al ., ; Cleary et al ., ; Radke et al ., ; Sullivan et al ., ). A seminal study generated multiple SAGE libraries to construct progressive ‘snapshots’ of the developmental transition from sporozoite to tachyzoite to bradyzoite in different Toxoplasma strains (Radke et al ., ).…”

Section: Triggers Of Bradyzoite Formationmentioning

confidence: 97%

Mechanisms ofToxoplasma gondiipersistence and latency

Sullivan¹,

Jeffers²

2012

FEMS Microbiol Rev

214

164

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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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Section: Triggers Of Bradyzoite Formationmentioning

confidence: 97%

Mechanisms ofToxoplasma gondiipersistence and latency

Sullivan¹,

Jeffers²

2012

FEMS Microbiol Rev

214

164

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show abstract

“…Once T. gondii infects humans and forms cysts during the chronic phase; encysted bradyzoites can rupture, reactivate into actively replicating and cytolytic tachyzoites, and cause symptomatic disease in immunocompromised individuals, such as people with HIV-AIDS or organ transplantation patients (Sullivan et al, 2009). It is also of importance to gain insight into how tissue Immune T cells from either wild-type or perforin knockout mice prevent BALB/c mice from toxoplasmic encephalitis and death (Wang et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Identification and co-localization of perforin-like (TgPLP1) protein in Toxoplasma gondii bradyzoites

Shan

Qian

Liu

et al. 2015

Experimental Parasitology

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“…A diferenciação de taquizoítos em bradizoítos é essencial para a patogênese e transmissão do T. gondii (SULLIVAN et al, 2009;BLANDER;SAEIJ, 2009). O desenvolvimento dos bradizoítos é um processo complexo que consiste em alterações transcricionais com modificações da cromatina que controlam a expressão de genes relevantes para induzir as condições de bradizoíto.…”

Section: Toxoplasma Gondiiunclassified

Mecanismos específicos de patogenicidade de protozoários intracelulares: Trypanosoma cruzi, Leishmania spp., Toxoplasma gondii e Plasmodium spp.

Barros¹,

Innocente²,

Silva³

et al. 2012

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Trypanosoma cruzi, Leishmania spp., Toxoplasma gondii e Plasmodium spp. apresentam mecanismos de patogenicidade que contribuem para a sobrevivência intracelular. O objetivo desta revisão é discutir os mecanismos patogênicos envolvidos na relação parasito-hospedeiro. Cada um desses protozoários possui mecanismos específicos para invasão, formação do vacúolo parasitóforo, desenvolvimento, obtenção de nutrientes e evasão do sistema imune. Dentre os fatores moleculares que contribuem para a virulência e patogenicidade destacamse as mucinas, a glicoproteína 160 e a cruzipaína para o T. cruzi; os lipofosfoglicanos e a glicoproteína de superfície principal para a Leishmania spp.; as proteínas das roptrias (ROP) e as proteínas quinases para o Toxoplasma gondii e as proteínas ROP, a proteína ligante de eritrócitos, o antígeno PfEMP1 (do inglês P. falciparum Erythocyte Membrane Protein-1) e a hemozoína para os Plasmodium spp. Os mecanismos descritos fornecem informações que contribuem para o entendimento dos processos patogênicos, assim como para descoberta de alvos terapêuticos e o planejamento de novos fármacos e métodos diagnósticos. Palavras-chave: Protozoários intracelulares. Mecanismos de patogenicidade. Relação parasito-hospedeiro.

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Understanding mechanisms and the role of differentiation in pathogenesis of Toxoplasma gondii: a review

Cited by 42 publications

References 54 publications

Mechanisms ofToxoplasma gondiipersistence and latency

Mechanisms ofToxoplasma gondiipersistence and latency

Identification and co-localization of perforin-like (TgPLP1) protein in Toxoplasma gondii bradyzoites

Mecanismos específicos de patogenicidade de protozoários intracelulares: Trypanosoma cruzi, Leishmania spp., Toxoplasma gondii e Plasmodium spp.

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