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Malaria is caused by infection with Plasmodium parasites. According to the World Malaria Report in 2016 there are over 200 million cases of malaria every year, resulting in approximately 500,000 deaths. Most of these deaths occur in children under 5 years, or in pregnant women. Given that the newly developed RTS,S has a transient and limited protection against Plasmodium infection and malarial disease, much work is still needed to develop novel therapeutics to help combat this disease.

Studying malaria in humans
There are 5 species of Plasmodium that infect humans, with Plasmodium falciparum and Plasmodium vivax being the most common causes of malaria cases worldwide. We work closely with Dr Lawrence Ayong and Dr Carole Eboumbou at the Center du Pasteur Cameroon in Central Africa, undertaking analyses of samples from children with malaria to determine.

Non-human primate malaria
We have also been heavily involved in non-human primate malaria research (Plasmodium cynomolgi in Rhesus macaques) by way of our involvement with MaHPIC at out of Emory University and our collaboration with Dr. Chet Joyner, UGA.

Mouse on bottle
Lab members at Centre Pasteur du Cameroun

Mouse models of malaria
We use mouse models of malaria to model different aspects of malarial disease. Plasmodium chabaudi and Plasmodium yoelii XNL cause non-lethal infections in C57BL/6 mice, and exhibit very similar features to human non-lethal malaria (anemia, temperature dysregulation and inflammatory immune responses). Our projects on vascular activation in cerebral malaria make use of the Plasmodium berghei ANKA model, commonly termed experimental cerebral malaria. We also use the Plasmodium berghei NK65 model of acute lung injury and malaria-associated respiratory distress syndrome. Recently funded work will use the Collaborative Cross mouse colonies to develop a genetically driven model of asymptomatic malaria.  

A long-standing interest in the Lamb lab has been the influence of co-infections on malaria pathogenesis.  

We are currently determining the molecular mechanisms by which gammaherpesviruse co-infection mediates the suppression of anti-malarial humoral immunity. We are using the well-established MHV68 mouse model of Epstein Barr Virus (EBV) infection. MHV68 has many similarities to EBV infection including acute and lytic phases of the life cycle and establishing latency in B cells.

Streptococcus: We are currently determining how pre-existing malaria can predispose children to Streptococcus pneumonia. We are using clinically derived isolates in mice that have pre-existing malaria as a model of severe Streptococcal disease.