PHILADELPHIA, PA -- Researchers at the University of Pennsylvania have discovered that parasites hijack host-cell proteins to ensure their survival and proliferation, suggesting new ways to control the diseases they cause. The study, appearing this week online in Science, was led by Doron Greenbaum, PhD, Assistant Professor of Pharmacology in the Penn School of Medicine.
"Researchers can now develop ways to kill parasites by placing roadblocks in the path they use to destroy their victims," says Greenbaum. The team discovered that malaria parasites depend upon an enzyme stolen from the host cell for successful infection. Historically, many researchers have focused on developing ways to keep parasites from entering host cells, but Greenbaum's group was curious about an alternative route of attack: locking the parasites inside the host cell.
These studies began with Plasmodium falciparum, which causes the most deadly form of human malaria. Each year, the Centers for Disease Control and Prevention report 350 million cases of malaria occur worldwide, killing more than a million people. In collaboration with the laboratory of Penn biologist David Roos, PhD, the work was broadened to include Toxoplasma gondii, which causes a parasitic disease called toxoplasmosis, the leading cause of birth defects worldwide and harmful to people with compromised immune systems. The CDC estimates more than 60 million people living in the U.S. carry T. gondii.
"We always suspected that enzymes called proteases might be required to help parasites escape from the infected cell, but had assumed that these enzymes were produced by the parasites themselves. We had never considered that parasites might instead hijack host cell proteases. It's an ingenious system," says Greenbaum. "Our findings open up whole new window for drug discovery."
"This work is a triumph of integrative science, combining modern tech
|Contact: Karen Kreeger|
University of Pennsylvania School of Medicine