Malaria parasites are able to disguise themselves to avoid the host's immune system, a new study has shown.
Malaria is caused by a parasite, which is injected into the bloodstream from the salivary glands of infected mosquitoes. There are a number of different species of parasite, but the deadliest is the Plasmodium falciparum parasite, which accounts for 90 per cent of deaths from malaria.
The malaria parasite infects healthy red blood cells, where it reproduces. The P. falciparum parasite generates a family of molecules, known as PfEMP1, that are inserted into the surface of the infected red blood cells.
The cells become sticky and adhere to the walls of blood vessels in tissues such as the brain. This prevents the cells being flushed through the spleen, where the parasites would be destroyed by the body's immune system, but also restricts blood supply to vital organs.
Each parasite has 'recipes' for around sixty different types of PfEMP1 molecule written into its genes.
However, the exact recipes differ from parasite to parasite, so every new infection may carry a set of molecules that the immune system has not previously encountered.
This has meant that in the past, researchers have ruled out the molecules as vaccine candidates.
However there appear to be at least two main classes of PfEMP1 types within every parasite, suggesting different broad tactical approaches to infecting the host. The most efficient tactic or combination of tactics to use may depend on the host's immunity.
Dr George Warimwe and colleagues from the Kenya Medical Research Institute (KEMRI)-Wellcome Trust Programme and the Wellcome Trust Sanger Institute, have shown that the parasites adapt their molecules depending on which antibodies it encounters in the host's immune response.
They have also found evidence to suggest that there may be a limit to the number of molecular types that are actually associated with severe disease.
The researchers studied malaria parasites in blood samples from 217 Kenyan children with malaria.
They found that a group of genes coding for a particular class of PfEMP1 molecule called Cys-2 tended to be switched on when the children had a low immunity to the parasite; as immunity develops, the parasite switches on a different set of genes, effectively disguising it so that immune system cannot clear the infection
Dr Peter Bull from the KEMRI-Wellcome Trust Programme and the University of Oxford, who led the research, said that the findings could suggest a new approach to tackling malaria, in terms of both vaccine development and drug interventions.
The study has been published in the journal Proceedings of the National Academy of Sciences.