Recent Advances in the Roles of Autophagy and Autophagy Proteins in Host Cells During Toxoplasma gondii Infection and Potential Therapeutic Implications

Toxoplasma gondii is an obligate intracellular protozoan that can cause encephalitis and retinitis in humans. The success of T. gondii as a pathogen depends in part on its ability to form an intracellular niche (parasitophorous vacuole) that allows protection from lysosomal degradation and parasite replication. The parasitophorous vacuole can be targeted by autophagy or by autophagosome-independent processes triggered by autophagy proteins. However, T. gondii has developed many strategies to preserve the integrity of the parasitophorous vacuole. Here, we review the interaction between T. gondii, autophagy, and autophagy proteins and expand on recent advances in the field, including the importance of autophagy in the regulation of invasion of the brain and retina by the parasite. We discuss studies that have begun to explore the potential therapeutic applications of the knowledge gained thus far.

Automated summary

Toxoplasma gondii is an intracellular protozoan that can cause encephalitis and retinitis in humans, depending on its ability to form a parasitophorous vacuole for protection and replication. The vacuole can be targeted by autophagy, but the parasite has developed strategies to preserve its integrity. Recent advances have highlighted the importance of autophagy in regulating invasion into the brain and retina by T. gondii, with potential therapeutic applications being explored.