Malaria drug resistance in Southeast Asia is caused by a single mutated gene in the disease-causing parasite, a Columbia University-led study has found.
"The bad news is that it shows that resistance can arise through single mutations in one gene and pop up anywhere, at any time," said David Fidock, professor of microbiology and immunology and of medical sciences at Columbia University.
This is 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.
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 in Southeast Asia.
No alternative therapy is currently available to replace ACTs.
The study, published in the journal Science, builds on a recent report that mutations in the gene -K13 - are frequently found in drug-resistant parasites in Southeast Asia.
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The good news is that K13 mutations produce a relatively weak resistance.
K13 mutations enable the parasite to hide in red blood cells in a developmental state that is naturally less vulnerable to artemisinin.
"This allows them to temporarily survive treatment, but it will not be enough for ACTs to fail across Africa, particularly as the partner drugs continue to be highly effective," Fidock noted.
But it may be a foundation for parasites to evolve stronger degrees of resistance to these therapies, so we have to watch for increasing resistance very carefully, he suggested.
This finding provides public health officials around the world with a way to look for pockets of emerging resistance and potentially eliminate them before they spread.