View an illustration about the life cycle of the malaria parasite.
John Adams, Ph.D., and colleagues at the Global Health Infectious Diseases Research Center, University of Florida, have developed an efficient method for inducing parasite transformation that is opening the door to new genetic studies of malaria parasites. Their collaborators in this work include researchers working in regions endemic for malaria, including southern Africa, Papua New Guinea, and South America.
In an NIAID-supported study, Dr. Adams and his team found that the malaria parasite protein known as MAEBL is critical for completing the life cycle of Plasmodium falciparum, the parasite responsible for 80 percent of all human malarial infections. The researchers genetically modified P. falciparum and fed them in a blood meal to uninfected mosquitoes. They found the parasites with deleted MAEBL were not in the salivary glands of the mosquitoes, even though they observed earlier forms of the parasites in the mosquitoes gut. The research team concluded that MAEBL is essential for the parasite to enter the mosquito’s salivary glands. Their findings suggest that silencing the receptor for MAEBL in the mosquito salivary gland might block passage of the parasite through the mosquito, thereby preventing human infection through the mosquito’s bite—essentially stopping malaria infection before it begins.
In other research, they discovered a new mutation in a gene for the Duffy blood group protein, which is located on the surface of red blood cells and acts as a receptor for the malaria parasite Plasmodium vivax. In non-human primates, this mutation reduces the susceptibility of red blood cells to malaria. Malaria caused by P. vivax is the major cause of clinical malaria outside of Africa. Targeting the parasite's Duffy binding protein, along with its interaction with the Duffy blood group, may be a productive strategy for developing a malaria vaccine for P. vivax.
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Last Updated June 18, 2009