'You can't afford to be 15 years behind the parasite'
As an undergraduate at Adelaide University in South Australia, David Fidock became interested in genetically engineering plants to make them resilient to increasing salinity and drought.
He wanted to do a Ph.D. focused on applying molecular biology techniques to improve health outcomes in the global south due to deteriorating climate conditions. So, he started applying for graduate positions in France and interviewed at several institutions.
His meeting with Pierre Druilhe, a physician–scientist at the Pasteur Institute in Paris, changed his life course.
Fidock was inspired by Druilhe’s work on developing a vaccine that would prevent malaria infection by targeting the parasite before it enters the host's bloodstream.
“From a values perspective, malarial work fits the same criteria as crop science — addressing global health needs through the application of molecular biology and experimental research,” Fidock said. “So, I decided to join his lab and contribute to malaria research instead.”
Margaret A. Phillips nominated Fidock for the 偷拍偷窥 and 偷拍偷窥 Biology’s 2025 Alice and C.C. Wang Award in 偷拍偷窥 Parasitology.
“Drug resistance has been a major contributor to our inability to control malaria on a global level,” Phillips wrote in her nomination letter, “and David’s work has had a major impact on our understanding of how drug resistance develops.”
Fidock is a professor at Columbia University and a member of the WHO’s Malaria Policy Advisory Group, which advises the Global Malaria Programme on its efforts to control and eliminate malaria, including a focus on combatting drug resistance.
“It's a huge, coordinated effort because we are now seeing the start of what could become a tsunami of resistance washing over Africa in coming years,” he said.
Identifying the genes responsible for drug resistance can take up to 15 years from the first signs that treatments are failing, providing ample time for resistant strains to emerge and spread.
“So how do you narrow this gap?” Fidock said. “You can't afford to be 15 years behind the parasite.”
Winning the race against a deadly species
Using tools such as genetic crosses between drug-resistant and susceptible parasites, combined with gene editing, Fidock’s research identifies the genetic and molecular basis of drug resistance in Plasmodium falciparum,the most lethal of the five human malaria parasite species.
Over the years, his lab has collaborated with the international public–private partnership Medicines for Malaria Venture to determine whether a preclinical candidate in the drug development pipeline is at a higher risk of acquiring parasite resistance. This helps increase the efficiency of the drug discovery and development process.
“We don't want to be working with compounds that select very easily for resistance,” Fidock said. “One of the major benefits of this type of research is to inform how we could rationally develop treatments, not only to cure malaria but to slow down its rate of acquiring multidrug resistance.”
The lab discovered that different mutations in the P. falciparum chloroquine resistance transporter develop resistance to the former first-line drug chloroquine and the current partner drug piperaquine. They saw that parasites resistant to piperaquine often lose resistance to chloroquine because of how the transporter mutations interact with these drugs.
“So, studying these inverse susceptibilities and combining both drugs could potentially block parasites from acquiring multidrug resistance,” Fidock said.
Fidock is focusing now on artemisinin-based combination therapies, how artemisinins work, identifying the cause of partial resistance to these therapies, and developing better treatments from drugs to strategies such as chemoprevention.
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