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RECENT EBOLA OUTBREAKS in the Republic of Congo and neighboring Gabon in central Africa have killed several dozen people. The virus’s mysterious appearances, rapid course and lack of treatment have made it a daunting challenge for public health — and a potential weapon for terrorists.
Now, a research team says it has answered important basic questions about how Ebola, and a related virus, Marburg, commandeer human cells. Their findings shed light on possible ways to design drug therapies. The Ebola virus, shaped like a shepherd’s crook, targets tiny fat platforms called “lipid rafts” that float atop the membrane of human cells. These cholesterol-rich rafts are the viruses’ gateway into cells, the assembly platform for making new virus particles, and the exit point where new virus particles bud. This virus-like particle, the harmless hollow shell of the Ebola virus, may one day be useful in creating an Ebola vaccine. The particle has been disarmed of its genetic material and is unable to replicate. Advertisement The team’s report, set to be published Monday in the Journal of Experimental Medicine, “is highly significant,” says Eric Freed, principal investigator in the laboratory of molecular microbiology at the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health in Bethesda, Md. “It adds another human pathogen to the growing list of viruses that use lipid rafts.” The findings add new insight into the life cycle of viruses and how they subvert human cellular mechanisms. It is a critical early step toward one day creating drugs that would stop viruses from replicating. Ebola and Marburg, both members of a family of hemorrhagic-fever viruses called filoviruses, share the reproduction strategy of viruses ranging from measles and influenza to HIV, which causes AIDS. Their ability to traffic aboard lipid rafts may help them evade the human immune system, researchers speculate. One of the researchers, Sina Bavari, at the U.S. Army Medical Research Institute of Infectious Diseases in Fort Detrick, Md., says, “By understanding how Ebola and Marburg are entering into and budding from the cells, it gives us an avenue to come up with new therapeutics that would alter these pathways.” Dr. Bavari’s co-author is M. Javad Aman, of Clinical Research Management Inc. in Frederick, Md.
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