Plasmodium falciparum resistance to artemisinin-based combination therapies (ACTs) started to crop up around 2007. Infections, especially in the Greater Mekong area of Southeast Asia, seemingly survived treatment. This was largely due to the pairing of artemisinin derivatives with older drugs that had existing resistance problems. But some experts think the emergence of partial resistance to artemisinin itself—which allows parasites to persist for longer in the body following treatment—could also play a role.
ACT of Resistance
Plasmodium falciparum resistance to artemisinin-based combination therapies (ACTs) started to crop up around 2007. This largely arose from pairing artemisinin derivatives with older drugs that had existing resistance problems. But the emergence of partial resistance to artemisinin itself—which allows parasites to persist for longer in the body following treatment—may also play a role.
Partial artemisinin resistance
Researchers have linked partial resistance to artemisinin-derived drugs with several mutations in the kelch13 gene,...
Partner drug resistance
In red blood cells, P. falciparum digests human hemoglobin to feed itself. In addition to amino acids, this releases toxic heme. Normally, the parasite polymerizes the heme into harmless clumps of hemozoin or degrades it through a handful of poorly understood pathways. But most ACT partner drugs inhibit detoxification. Some partner drugs also attack the parasite through other mechanisms. Here are examples of how P. falciparum strains resist these drugs.
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