LOS ANGELES, CA (Embargoed until 5 p.m. EST on September 2, 2002) For decades, scientists have tried to figure out how to stop viruses from spreading. Their efforts have led to the development of drugs that can help to slow the spread of some infections and diseases such as AIDS by preventing viruses from reproducing. But because viruses' genetic machinery has the ability to replicate and mutate so quickly, viruses rapidly become resistant to individual anti-viral drugs. Thus, the effectiveness of these drugs is very limited.

Now, researchers currently at Cedars-Sinai Medical Center, and the Universidad Autonoma de Madrid, in Spain, report that treating a common virus with a mutation-causing cancer drug caused the virus to mutate so much that it was no longer able to reproduce and was driven to extinction. The findings, reported in the current issue of the Proceedings of the National Sciences (PNAS), and preceded by a Commentary by Nobel-Prize winning Professor Manfred Eigen from the Max Planck Institut fur biophysikalische Chemie, Goettingen, Germany, may ultimately lead to new ways to treat and eliminate viral infections.

"We found that a specific chemical mutagen caused the virus to mutate so much that the replication process was ultimately aborted," said Pedro Lowenstein, M.D., Ph.D., Director of the Board of Governor's Gene Therapeutics Research Institute at Cedars-Sinai Medical Center. "These findings, may lead, in the future, to ways to stop viruses from reproducing in humans in the same way."

"Although the possibility to exploit high mutation rates in viruses was already known, this and other work is providing the basis for more rapid progress in this field," said collaborator and co-author Esteban Domingo, Ph.D, Director of the Laboratory of Genetic Variability of RNA Viruses at the Center for Molecular Biology 'Severo Ochoa', Universidad Autonoma de Madrid, Spain.

Viruses are genetic entities that can cause a number o
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Contact: Kelli Stauning
kelli.stauning@cshs.org
310-423-3674
Cedars-Sinai Medical Center
2-Sep-2002

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