Parasites are subversive; they bend their environment to their own ends. Plasmodium falciparum and Toxoplasma gondii are two of a large group of single-celled parasites (the Apicomplexa) that invade host cells and hijack the normal biology of those cells to support their own development.

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In the case of Plasmodium. falciparum, the parasite that causes malaria, this has severe consequences: more than 400,000 people die of malaria each year, and more than 200 million people are infected. Despite being so widespread, Plasmodium falciparum is a specialist: it has very limited host cell type and species specificity. 

 

Toxoplasma gondii, in contrast, is a generalist: it can infect any nucleated cell of any warm blooded species - including humans. It is estimated that about 30% of the world's population is infected with Toxoplasma. In most people, this infection is dormant because it is controlled by the immune system, but it is never completely cleared. In pregnant or immune-suppressed individuals, however, Toxoplasma can become a real threat: it can cause severe problems in developing foetuses, and untreated infection in immune-compromised individuals can result in severe eye and brain damage, or even death. 

 

These two parasites live in very different biological niches, but immune evasion, host cell remodelling, and adaptions to enable transmission between hosts are key to both of their parasitic lifestyles. Our main aim is to determine how the parasites remodel their hosts to for survival, immune evasion, and dissemination. The key tools we use for this are quantitative mass spectrometry, which allows us to interrogate protein interactions and modifications that underpin these processes, and CRISPR-Cas9 based knockout screening, to assess the functional contribution of hundreds of different proteins at the same time. Together with other biochemical, cell biological, and genetic tools, these technologies allow us to uncover exciting and novel biology to build the basis for future therapeutic strategies.

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