When viruses attack, one molecule more than any other fights back. Interferon triggers the activation of more than 350 genes, and despite the obvious connection, the vast majority have never been tested for antiviral properties. A team of researchers, led by scientists from Rockefeller University, for the first time has carried out a comprehensive, systematic evaluation of the antiviral activity of interferon-induced factors. The findings, published online today in the journal Nature, are a first step toward unraveling how these naturally occurring molecules work to inhibit viruses.
"We hope this study will open the door to future work on the mechanisms of antiviral molecules," says first author John Schoggins, a postdoctoral associate in Charles M. Rice's Laboratory of Virology and Infectious Disease at Rockefeller. "Such mechanistic studies may set the stage for the development of new and much needed drugs to combat a diverse array of viruses that pose significant health threats to people worldwide."
The researchers were interested in type I interferon, a cellular molecule that is made when a person becomes infected with certain viruses. Type I Interferon is used clinically in the treatment of some viral diseases, such as hepatitis C, and its presence has been shown to significantly limit the severity of certain viral infections.
Schoggins and his colleagues, including researchers from the Aaron Diamond AIDS Research Center and the Howard Hughes Medical Institute, systematically evaluated the majority of common interferon-induced genes, one by one, to determine which of them had antiviral activity against a panel of disease-causing viruses, including the hepatitis C virus, HIV, West Nile virus, the yellow fever virus and chikungunya virus.
The scientists used a cell-based "screen" to measure the ability of each gene to halt the growth of the viruses: One by one, genes were delivered into the cells that were then inf
|Contact: Joseph Bonner|