Malaraia parasistes isolated in Rwanda have mutations conferring resistance to a front-line drug.
Resistance to the gold-standard malaria treatment, the drug artemisinin, has been rising in southeast Asia for a decade — and there is evidence that artemisinin-based therapies might start to fail in Rwanda, too.
In Asia, artemisinin drug resistance has been linked to various mutations in the ‘K13’ section of the genome of the most deadly malaria parasite, Plasmodium falciparum. Aline Uwimana at the Rwanda Biomedical Centre in Kigali, Didier Menard at the Pasteur Institute in Paris and their colleagues detected K13 mutations in P. falciparum parasites collected from people with malaria in Rwanda.
The team genetically modified parasites to harbour the changes conferred by the mutations. These bioengineered parasites were resistant to artemisinin in the laboratory.
However, malaria therapies consisting of artemisinin combined with other drugs successfully treated people in Rwanda infected with P. falciparum — including P. falciparum that has the K13 mutations. The researchers suggest that the other drugs helped the infected people to recover.
A genetic analysis suggests that parasites with the mutation didn’t arrive from Asia, but arose independently in Africa. By contrast, mutations that rendered P. falciparum resistant to a former malaria treatment, chloroquine, seem to have spread to Africa from Asia — resulting in millions of childhood deaths.