Though malaria deaths have dropped by 30 percent worldwide since the introduction of artemisinin-based combination therapies (ACTs) in the late 1990s, these gains are now threatened by the emergence of resistance to the core artemisinin component of ACTs in Southeast Asia.
No alternative therapy is currently available to replace ACTs should resistance spread to other parts of the world.
The study, published in Science, builds on a recent report that mutations in the gene K13 are frequently found in drug-resistant Plasmodium falciparum parasites in Southeast Asia.
Researchers led by David Fidock, professor of microbiology & immunology and of medical sciences (in medicine) at Columbia University Medical Center working with scientists at the Pasteur Institutes in Paris and Cambodia, the University of Toulouse III, Sangamo Biosciences Inc, and the National Institutes of Health, showed definitively that K13 mutations directly cause drug resistance.
"The bad news about our finding is that it shows that resistance can arise through single mutations in one gene and pop up anywhere, at any time," Fidock said.
"That's quite different from past instances with former first-line drugs, when complex sets of multiple mutations were required and resistance spread only as the mutated parasites spread," he said.
The good news is that K13 mutations produce a relatively weak resistance. A related study published in the same issue of Science found that K13 mutations enable the parasite to hide in red blood cells in a developmental state that is naturally less vulnerable to artemisinin.
Field reports suggest that not all K13 mutations are capable of causing resistance, and Fidock believes the genetic system developed by him to study K13, based on DNA repair approaches that are being used in human gene therapy studies, will be critical in identifying real hot spots of resistance.

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