Tham Lab

In the human host, complement regulators modulate the complement cascade to protect self-tissue from indiscriminate complement attack. Pathogens, on the other hand actively recruit host regulators with the foremost intention of inhibiting the complement cascade to prevent pathogen destruction. The acquisition of host complement regulators is the most widely used strategy for complement evasion among viruses, bacteria, fungi and parasites. This project will involve identifying which complement regulators are recruited by malaria parasites and how this prevents killing. It will also investigate the role of parasite surface proteins in recruitment of human complement regulators. This project will provide the first identification of complement evasion strategies employed by the malaria parasite.

Being an obligate intracellular parasite, malaria parasites have to invade red blood cells in order to survive within the human host. One essential step within invasion is the recognition of human red blood cells by malaria parasites, a process involving an intimate interaction between parasite adhesins and red blood cells receptors. This project will identify novel parasite adhesins involved in red blood cell recognition and how they function in the dynamic process of entry. We can exploit this information to rationally design inhibitors or antibodies to prevent malaria parasite invasion into human red blood cells.

Our lab is interested in identifying novel parasite adhesins involved in red blood cell recognition and how they function in the dynamic process of parasite entry.

This project will involve characterisation of human monoclonal antibodies to identify neutralising antibodies that effectively inhibit parasite invasion. We will use a wide range of biochemical, structural and molecular techniques to characterise the mechanism of inhibition. We can exploit this crucial information to rationally design a potential vaccine to prevent malaria parasite invasion into human red blood cells.