Brown researchers link px1 gene mutations to rising malaria drug resistance in Uganda
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Brown University researchers identified mutations in the px1 gene as a likely driver of rising drug-resistant malaria in Uganda. Whole-genome analysis of 157 parasite samples collected from 2016 to 2024 showed the PIN mutation cluster spread rapidly, reaching 84% prevalence in northern Uganda by 2024. The mutation reduced parasite sensitivity to lumefantrine, a key component of the common artemether-lumefantrine treatment.
Key Facts
- The PIN mutation cluster in the px1 gene was first detected in a 2008 sample from Uganda.
- By 2024, PIN prevalence reached 84% in northern Uganda and 55% in eastern Uganda.
- Malaria parasites carrying PIN showed reduced sensitivity to lumefantrine and other antimalarials.
- The study analyzed 157 malaria parasite samples collected in Uganda between 2016 and 2024.
Genetic Analysis
Researchers conducted whole-genome analysis of 157 malaria parasite samples from Uganda collected between 2016 and 2024. The team identified a cluster of three amino acid mutations and two deletions in the px1 gene, naming it PIN. Parasites carrying PIN passed on a large region surrounding px1 almost entirely intact, indicating rapid recent spread. Historical sample analysis confirmed the PIN mutation first appeared in a 2008 specimen.
Drug Resistance Impact
Experiments showed PIN-carrying parasites exhibited reduced sensitivity to lumefantrine, a component of artemether-lumefantrine. The mutation also reduced sensitivity to other antimalarial drugs. Researchers confirmed the effect by testing parasites with intentionally disrupted px1 genes. Jeffrey Bailey, associate professor at Brown University, warned that drug resistance could undermine malaria control and lead to more deaths.
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Brown researchers link px1 gene mutations to rising malaria drug resistance in Uganda
