Toxoplasma gondii is an obligate intracellular parasite, which chronically infects one third of the world’s population and results in the development of parasitic cysts within the brain. The parasite actively manipulates their host by exporting proteins during the acute tachyzoite stage. In contrast, little is known on whether the chronic cyst-bradyzoite stage manipulates the host by similar means and if the parasite is actively responsible for the changes observed in animal behaviour studies. Correlative links between T. gondii specific antibodies in humans and a range of psychiatric and mental health disorders, such as schizophrenia and depression, has created a need to understand how chronic T. gondii modifies infected neurons and how this affects human psychology. I used RNA sequencing to show that the transcriptional profile of the host cell is strikingly different between bradyzoite and tachyzoite infected cells. To further distinguish the effects between parasitic and host immune factors, I have created a transgenic parasite line defective in protein export. Together this data has enabled us to demonstrate that bradyzoite specific proteins must be exported into the host cell to modulate the host’s transcriptome. In addition, preliminary western blot data suggests that known tachyzoite effectors are expressed during the bradyzoite stages and may continue their manipulation into the chronic stages. Ultimately, this export-defective line will be used in mouse behavioural studies to determine if protein export during chronic T. gondii infection affects behaviour. In understanding how T. gondii cysts export proteins and manipulate the host cell, we aim to gain insight on how chronic infection of the brain, and resulting immune responses, can impact mental health and brain physiology.