Excreted/secreted antigens of Toxoplasma gondii — their origin and role in the host-parasite interaction

1993 ◽  
Vol 144 (1) ◽  
pp. 41-44 ◽  
Author(s):  
M.F. Cesbron-Delauw ◽  
A. Capron
2017 ◽  
Vol 1 (6) ◽  
pp. 563-572 ◽  
Author(s):  
Pierre-Mehdi Hammoudi ◽  
Dominique Soldati-Favre

Typically illustrating the ‘manipulation hypothesis’, Toxoplasma gondii is widely known to trigger sustainable behavioural changes during chronic infection of intermediate hosts to enhance transmission to its feline definitive hosts, ensuring survival and dissemination. During the chronic stage of infection in rodents, a variety of neurological dysfunctions have been unravelled and correlated with the loss of cat fear, among other phenotypic impacts. However, the underlying neurological alteration(s) driving these behavioural modifications is only partially understood, which makes it difficult to draw more than a correlation between T. gondii infection and changes in brain homeostasis. Moreover, it is barely known which among the brain regions governing fear and stress responses are preferentially affected during T. gondii infection. Studies aiming at an in-depth dissection of underlying molecular mechanisms occurring at the host and parasite levels will be discussed in this review. Addressing this reminiscent topic in the light of recent technical progress and new discoveries regarding fear response, olfaction and neuromodulator mechanisms could contribute to a better understanding of this complex host–parasite interaction.


2019 ◽  
Vol 120 (9) ◽  
pp. 16044-16051 ◽  
Author(s):  
Jinling Chen ◽  
Liang Hu ◽  
Jingjing Wang ◽  
Yangqing Cao ◽  
Dandan Zhu ◽  
...  

2018 ◽  
Vol 119 (12) ◽  
pp. 10176-10185 ◽  
Author(s):  
Jinling Chen ◽  
Caiqun Huang ◽  
Dandan Zhu ◽  
Liuting Chen ◽  
Jianxin Wang ◽  
...  

Author(s):  
Ellen Tedford ◽  
Glenn McConkey

Although the parasite Toxoplasma gondii is one of the most pervasive neurotropic pathogens in the world, the host-parasite interactions during CNS infection and consequences of neurological infection are just beginning to be unraveled. The chronic stages of infection have been considered dormant, although several studies have found correlations of infection with an array of host behavioral changes. These may facilitate parasite transmission and impact neurological diseases. During infection, in addition to the presence of the parasites within neurons, host-mediated neuroimmune and hormonal responses to infection are also present. T. gondii induces numerous changes to host neurons during infection and globally alters host neurological signaling pathways, as discussed in this review. Understanding the neurophysiological changes in the host brain is imperative to understanding the parasitic mechanisms and to delineate the effects of this single-celled parasite on health and its contribution to neurological disease.


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