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• W2677736497 abstract "Globally, nearly 2 billion people are infected with the intracellular protozoan Toxoplasma gondii1. This persistent infection can cause severe disease in immunocompromised people and is epidemiologically linked to major mental illnesses2 and cognitive impairment3. There are currently no options for curing this infection. The lack of effective therapeutics is due partly to a poor understanding of the essential pathways that maintain long-term infection. Although it is known that Toxoplasma replicates slowly within intracellular cysts demarcated with a cyst wall, precisely how it sustains itself and remodels organelles in this niche is unknown. Here, we identify a key role for proteolysis within the parasite lysosomal organelle (the vacuolar compartment or VAC) in turnover of autophagosomes and persistence during neural infection. We found that disrupting a VAC-localized cysteine protease compromised VAC digestive function and markedly reduced chronic infection. Death of parasites lacking the VAC protease was preceded by accumulation of undigested autophagosomes in the parasite cytoplasm. These findings suggest an unanticipated function for parasite lysosomal degradation in chronic infection, and identify an intrinsic role for autophagy in the T. gondii parasite and its close relatives. This work also identifies a key element of Toxoplasma persistence and suggests that VAC proteolysis is a prospective target for pharmacological development. Disruption of a cysteine protease that localizes to the vacuolar compartment of Toxoplasma gondii shows that autophagy is required for the intracellular survival of the parasite during chronic infection." @default.
• W2677736497 created "2017-06-30" @default.
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• W2677736497 date "2017-06-19" @default.
• W2677736497 modified "2023-10-17" @default.
• W2677736497 title "Toxoplasma depends on lysosomal consumption of autophagosomes for persistent infection" @default.
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• W2677736497 doi "https://doi.org/10.1038/nmicrobiol.2017.96" @default.
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