New Mutations in P. vivax Malaria Parasite May Increase Human Susceptibility

Researchers at Case Western Reserve University and Cleveland Clinic Lerner Research Institute have discovered recent genetic mutations in a parasite that causes over 100 million cases of malaria annually—changes that may render tens of millions of Africans who had been considered resistant, susceptible to infection. Dr. Peter A. Zimmerman, professor of international health, biology, and genetics at the Case Western Reserve School of Medicine, and Dr. David Serre, a scientific staff member of the Genomic Medicine Institute at Lerner and assistant professor of genomics at Case Western Reserve, report their findings at the American Society of Tropical Medicine and Hygiene annual meeting today, Friday, November 15, 2013. They and fellow researchers describe the changes in the Plasmodium vivax genome in papers scheduled to be published in the journal PLoS Neglected Tropical Disease on November 21 and December 5, 2013. To learn the functions of the mutations, and whether the parasite is evolving around a natural defense, Drs. Zimmerman and Serre have received a $3.5 million grant from the National Institute of Allergy and Infectious Disease at the National Institutes of Health. They will begin their field study in early 2014. "We've found a duplication of a gene known to enable the parasite to infect red blood cells and two possible additional components to a more complex red cell invasion mechanism," Dr. Zimmerman said. Researchers have long thought that P. vivax infects a person one way: a protein on the parasite, called the Duffy binding protein, latches onto a Duffy receptor on the surface of the person's red blood cell and works itself through the membrane. People who lack the receptor are called Duffy-negative and are resistant to infection.
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