Nels Elde, a 2012 Pew scholar and assistant professor of evolutionary genetics at the University of Utah, has led a study revealing a 40-million-year evolutionary clash between bacteria and their hosts. The findings, published Dec. 11 in Science, examined transferrin, a protein which collects and transports the nutrient iron.
Iron is essential for both the growth of human cells and for the survival of most infectious organisms, such as the pathogens that cause meningitis. Bacterial meningitis can be the result of infection by several strains of bacteria and leads to thousands of deaths every year. Those pathogens survive by prying open transferrin and stealing the iron stored inside.
Elde’s investigation of transferrin—proposed in his application to the Pew Scholars Program in the Biomedical Sciences—aims to understand the protein’s strategies for protecting its cargo. He has since found that transferrin has undergone myriad changes over the past 40 million years, mostly in an area that came into contact with these deadly bacteria. As transferrin focused its adaptations on the point of contact with bacteria, the thieving pathogens countered these defenses with changes to their own structures. Elde has observed this evolutionary response in at least two of the bacterial strains responsible for meningitis.
He also explored differences among primate species and discovered that transferrin from chimpanzees—our closest relatives—is more effective at holding onto iron atoms than the human form.
“Once we saw the difference with chimps, we thought: We should really look at human diversity,” he said to National Geographic. “And we didn’t have to look far.” He found that up to one-quarter of people have a newly evolved form of transferrin more adept at starving bacteria of iron than the variant the rest of the human population possesses.
Elde’s work illuminates an effective strategy of preventing infectious disease and circumventing antibiotic resistance, and it may lead to a new arsenal of antibiotic therapeutics based on transferrin.
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