Two new genetic studies of a parasite that causes malaria suggest that it may evolve new ways of invade human blood cells. The development could make some more dangerous parasite strains for people who have some natural immunity. Now about 95% of people in sub-Saharan Africa, where the malaria burden is highest are considered resistant to the parasite in question, Plasmodium vivax . If the parasite was to overcome their genetic defense against disease, it would potentially threaten hundreds of millions of people than it does today.
Vivax malaria is widespread in Asia and South America. Although less deadly than its cousin Plasmodium falciparum , which causes most malaria deaths, P. vivax beginning to be recognized as an important cause of serious diseases worldwide. To enter human blood cells, the parasite usually uses said protein Duffy blood group, a protein on the surface of red blood cells. But because up to 95% of the population across sub-Saharan Africa has the protein a genetic trait called "negative Duffy" -They have long been thought to be protected against infection. However, reports have emerged in recent years of Duffy-negative people who are still infected with vivax malaria. Peter Zimmerman of Case Western Reserve University in Cleveland, Ohio, and colleagues found, for example, that nearly 10% of Duffy-negative patients in Madagascar that have clinical malaria were infected P. vivax .
Now Zimmerman and his colleagues found a genetic clue that may help explain clinical observations. They sequenced the genomes of several P. vivax strains from patients in Madagascar and found that they had two copies of the gene that encodes the protein binding Duffy. Duplication occurred at higher rates in areas where relatively Duffy-negative patients vivax malaria, researchers reported this morning at the American Society of Tropical Medicine and Hygiene annual meeting in Washington, DC
Because P. vivax can not be grown in the laboratory, it is difficult to test how the extra copy of the gene could change the behavior of the parasite. But Zimmerman thinks that duplication can somehow help the parasite to invade blood cells Duffy-negative. It's still just an association, he said, but "two things happen in Madagascar that are unusual in the world," Duffy-negative infections and gene duplication. The genetic signature of the additional copy suggests that it may be a relatively new mutation, he said.
In a second study presented at the meeting this morning, David Serre of the Institute of Genomic Medicine of the Cleveland Clinic said that he and his colleagues have discovered a previously unidentified gene in P. vivax strain of Cambodia seems encode another protein that helps the parasite invades the blood cells. The gene is present in strains from around the world, but it lacks the first strain of P. vivax sequencing, which provided the "reference strain" for the species. It was a strain that had adapted to infect laboratory monkeys, because the parasite can not be grown in the laboratory. Serre says the parasite tamed laboratory may have lost the gene, which is why it was not found in the sequence reference. the gene may also play a role in the Duffy-negative infections, he said.
This is "biologically plausible," says Kevin Baird of the clinical research Unit Eijkman-Oxford in Jakarta . But it is not yet clear whether the Duffy-negative infections are an emerging phenomenon or have been present undetected, all along. "it is certainly cause for concern and merits further investigation," he said.
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