How malaria outwits our immune system
17 Dec 2009 by Evoluted New Media
Malaria parasites dupe their host’s immune system by adapting their molecules depending on the antibodies encountered according a recent study into the disease.
Malaria parasites dupe their host’s immune system by adapting their molecules depending on the antibodies encountered according a recent study into the disease.
The study – which examined malaria parasites in blood samples from 217 infected Kenyan children – may provide fresh approaches to tackling the disease in terms of vaccine development and drug interventions.
“The malaria parasite is very complex, so our immune system mounts many different responses, some more effective than others and many not effective at all,” said Dr Peter Bull from the Kenya Medical Research Institute-Wellcome Trust Pr¬ogramme and the University of Oxford, who led the research.
Malaria parasites are injected into the blood stream from the salivary glands of infected mosquitoes and infect healthy red blood cells where they reproduce. The most deadly, Plasmodium falciparum generates a family of molecules known as PfEMP¬1 that are inserted into the surface of the infected cell. It causes cells to become sticky and adhere to the walls of blood vessels, restricting supply to vital organs. This prevents them from being flushed through the spleen and destroyed.
Each parasite has the code for around 60 different types of PfEMP1 written into its genes, but the exact code varies from parasite to parasite, so each new infection could have a different set of molecules not encountered by the body. However, it appears there are two main classes of PfEMP1 within every parasite suggesting a broad tactical approach to infecting the host.
The study found that a group of genes coding for a particular type of PfEMP1 called Cys-2 tended to be switched on when the children had low immunity to the parasite and as immunity develops, a different set of genes is switched on, disguising the parasite so the immune system cannot clear the infection.
Dr George Warime and colleagues also found an independent association between activity in Cys-2 genes and severe malaria in children, suggesting specific forms of the molecule are more likely to trigger specific disease symptoms. He also suggests that there may be a limit on the number of molecule types that are associated with severe disease.
Dr Bull suggests the findings could lead to new approaches for tacking. “If there exists a limited class of severe disease-causing variants that naturally-exposed children learn to recognise readily this opens up the possibility of designing a vaccine against severe malaria that mimics and adult’s immune response, making the infection less dangerous,” he said.
