Malaria infection begins when an infected female Anopheles mosquito bites a person, injecting Plasmodium parasites, in the form of sporozoites. Sporozoites are formed in the midgut of the mosquito, where they emerge from oocysts and reach the salivary gland. Minutes after the mosquito bite, malaria sporozoites enter hepatocytes. During the liver stage, a single Plasmodium sporozoite invades a hepatocyte and gives rise to thousands of merozoites, which initiate blood-stage infection. We are particularly interested in the mosquito borne sporozoite stage of the parasite, its infection, and its development in the liver.
Nearly half the world's population lives in areas at risk of malaria transmission in 91 countries and territories. About 200 million cases and 400,000 deaths are reported annually due to malaria worldwide. Despite the progress achieved towards malaria burden reduction, the factors responsible for sporozoite infection in the liver is not well understood, which impairs the combat against this deadly disease.
The broad goal of our research is to understand the basic mechanisms regulating Plasmodium infection and maturation in the liver. Our current work focuses on ApiAP2 transcription factors and Autophagy proteins regulating these processes. Using reverse genetic approaches, cell biology, biochemistry, and in vivo models, we explore the parasite’s developmental stages and interactions with the host. A better understanding of the mechanistic links between parasite proteins and growth control may ultimately lead to better treatment
Our research also involves the development of genetically attenuated malaria parasites (GAP) as a vaccine. Using a rodent malaria model Plasmodium berghei, we have identified and characterized new Plasmodium genes essential for liver stage development. Currently, we are deciphering the attenuation mechanism and analyzing the immune parameters induced by GAPs.