"Resistance to antimalarial medication threatens the health of more than half of the world's population," notes corresponding Paul Roepe, PhD, a Georgetown chemistry professor who authored the study with colleagues at the University of Notre Dame and the University of Kentucky. Many antimalarial drugs both slow the growth of malarial parasites, and, at higher doses or over longer periods of time, also kill the malarial parasites. "Until now, no studies have separated how resistance to these two different drug actions might work," says Roepe, also a professor of biochemistry and cell and molecular biology and co-founder of Georgetown's Center for Infectious Disease at Georgetown University Medical Center.
"Our study found genetic and cell biological evidence linking autophagy to resistance to the parasite, which kills the effects of drugs."
Important Implications Autophagy, Roepe explains, is the process by which cells remove damaged parts of themselves to restore normal function. In this case, the cell rids itself of the parts damaged by the antimalarial drug. Roepe worked with two alumni of the chemistry Ph.D. program, David Gaviria (G'13) and Michelle Paguio (G'09), as well as current student Ph.D. chemistry student Amila Siriwardana (G'16) on the research.
The professor and his colleagues demonstrated in their study that while resistance to drugs like chloroquine, which works to slow the growth of malaria, has been explored, an explanation of the resistance to the cell-destroying effects of the medication has not been fully understood. "These results have important implications in the ongoing development of new antimalarial drug therapy," Roepe says. "We hope that by publishing this work in an open access journal, more researchers will access it and can expedite drug development.
Source: Eurekalert
