“We African scientists research malaria because we live the problem.”<\/p>\n
Abdoulaye Djimd\u00e9, Professor of parasitology and mycology, University of Sciences, Techniques, and Technologies of Bamako<\/p>\n
Share \u201cIn the Global North, colleagues tend to work with what I call pet parasites\u2014parasites that have been in the lab for 30 years, adapted to lab conditions, grown and regrown so many times that their features are sometimes different from what you find in patients today,\u201d Djimd\u00e9 says.<\/p>\n Working with current field isolates, his team reaches conclusions about drug candidates that diverge sharply from findings made in labs that use only laboratory models. For example, a study Djimd\u00e9\u2019s lab published recently compares how well 14 antimalarial drugs performed<\/a> against Plasmodium falciparum, the deadliest malaria parasite spread by mosquitoes (J. Antimicrob. Chemother.-Antimicrob. Resist. 2026, DOI: 10.1093\/jacamr\/dlag015). The team noticed significant differences in drug responses and linked those to each of three sites the parasites had been collected from. The variability the researchers found in drug resistance could inform treatment strategies in each region, the researchers report.<\/p>\n That focus on field research had defined Djimd\u00e9\u2019s work from the beginning. His doctoral research at the University of Maryland, Baltimore, led him to investigate why chloroquine, the frontline drug against malaria for decades, had stopped working in sub-Saharan Africa starting in the 1970s<\/a>. In the 1990s, he and colleagues tested how effective chloroquine was in treating uncomplicated cases of malaria in rural Mali.<\/p>\n The root cause of the resistance lay in a gene\u2014not one in humans but in the parasite\u2019s DNA. Between 1996 and 2001, he worked as a visiting fellow with scientists at the National Institutes of Health (NIH) to identify a mutation in one of the parasite\u2019s genes, a section of DNA that codes for the protein Plasmodium falciparum chloroquine-resistant transporter, or PfCRT. The NIH team found that the mutated protein stopped chloroquine from entering the parasite\u2019s vacuole<\/a>, where the drug would otherwise kill the bug (Mol. Cell 2000, DOI: 10.1016\/S1097-2765(05)00077-8).<\/p>\n Djimd\u00e9’s team then validated the mutation in the field in Mali<\/a>, treating malaria patients with chloroquine and screening surviving parasites for the mutation (N. Engl. J. Med. 2001, DOI: 10.1056\/NEJM200101253440403). Every resistant parasite carried it; every susceptible one did not. \u201cThat was really the first validation of this point mutation in the field,\u201d Djimd\u00e9 says.<\/p>\n The group then developed an assay that required only a dried blood spot on filter paper\u2014no cold chain or specialist equipment needed\u2014and that could be mailed like a normal letter. The mutated gene became the most widely used molecular tool for tracking chloroquine resistance globally.<\/p>\n The approach of taking a complex scientific finding and making it work in the field with minimal resources is what Djimd\u00e9 brings to the UN advisory board, where he argues that scientific innovations must be judged by whether they can reach the people who need them most.<\/p>\n By the early 2000s, large international genomics consortia were generating population-level data on P. falciparum from across the world. A conclusion kept surfacing: African parasite populations showed low genetic diversity. Compared with parasites from Asia or Latin America, African parasites appeared uniform. In the language of those public health meetings, they were the negative control\u2014scientifically uninteresting.<\/p>\n \u201cWe used to attend these meetings and think, That is not the full story. We knew that malaria behaved differently in different parts of the continent,\u201d Djimd\u00e9 says. \u201cAnd we knew that must have been driven by genetic differences.\u201d<\/p>\n In 2013, Djimd\u00e9 and a group of other African scientists formally launched the Plasmodium Diversity Network Africa, now called the Pathogen Genomic Diversity Network Africa. The group eventually assembled and analyzed parasite genes\u2014all collected from the field\u2014from 15 African countries.<\/p>\n The results overturned the consensus. Parasites from southern, central, eastern, and western Africa were all genetically distinct from each other. \u201cIt completely changed the way the field thought about and studied African parasites,\u201d Djimd\u00e9 says.<\/p>\n He had to create an entirely Africa-led research network just to ask the right questions, something Djimd\u00e9 says informs his outlook as he begins work with the UN. Science governance, he argues, has the same problem genomics had: the frameworks are built without African input, and the blind spots follow.<\/p>\n While building the network, Djimd\u00e9 became involved in one of the most consequential problems in malaria drug development. Pyramax, a combination drug, had shown strong efficacy even against resistant strains of malaria, but early trials flagged liver toxicity cases. As part of its approval of Pyramax in 2012, the European Medicines Agency restricted it to a single lifetime dose<\/a>, pending more data.<\/p>\n For a continent where children suffer several malaria episodes per year, that was effectively a disqualification. \u201cA drug that you can only use once in a lifetime is not a drug for Africa,\u201d Djimd\u00e9 says.<\/p>\n Between 2011 and 2016, his team tracked patients across repeated infections, working with a West African clinical trials network, Pyramax\u2019s South Korean codeveloper, and the nonprofit and drug codeveloper Medicines for Malaria Venture. Each patient was followed for 2 years, a novel design at the time.<\/p>\n
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