My research interests focus on the molecular mechanisms by which the malaria parasite is able to avoid host immunity and adapt to changes in the host cell environment. One of the main problems in developing an efficient malaria vaccine is the ability of the parasite to evade host immune responses. Immune evasion happens both at the level of the infected red blood cell and at the process of invasion, the step at which the parasite infects a new cell.

A key focus area of the lab is to understand the mechanisms on how the malaria merozoite recognizes and penetrates the erythrocyte. To address these questions we have particular focused on the role of the Reticulocyte Binding Protein Homologues (RH) family of proteins which is found in all malaria species and has been implicated on playing a role in immune evasion and parasite virulence. Using both the human parasite Plasmodium falciparum as well as the rodent parasite P. yoelii we have been able to address question relating to mechanisms regulating parasite virulence as well as getting a cleared understanding on how these large proteins mediate their function. An interesting upshot of this work is the possibility of using them as part of a malaria vaccine formulation.

In addition to merozoite invasion the lab has also spend significant effort in elucidating the biological role of the STEVOR and PIR multigene families identified in P. falciparum and P. vivax respectively. While STEVOR is unique to P. falciparum the PIR multigene family is found not only in P. vivax, but also rodent and simian malaria parasites. My research group has focused on developing a range of reagents that allow us to address what the role of STEVOR is in parasite development. We have recently been able to show that STEVOR is important for immune evasion and plays a direct role in parasite mediated rosetting. The PIR gene family provides a unique opportunity to study antigenic variation in a rodent model and possibly utilize the information gained in this system to understand how these genes may work in the intractable human parasite P. vivax. Currently, our efforts focus on understanding how the pir genes are transcriptionally regulated.
At the same time my research group has expanded to also focus more on the host responses in relation to parasite infections. This has identified NK cells as critical in protecting the host from parasite induced virulence. In addition we have developed a wide range of omic tools to study the parasite in more detail. Using these platforms has provided new insights in P. vivax biology and has identified RNA modifications as an important regulator of gene expression.