Most people know that cigarettes and high-fat food can contribute to atherosclerosis, the leading killer in the developed world. But is an unhealthy lifestyle all it takes to clog arteries? A small but vocal group of researchers believes atherosclerosis starts with a virus, not a cheeseburger. According to the theory, vascular damage caused by a virus could lay a foundation for the build-up of plaque.

Though it has its supporters, this theory has always suffered a credibility problem -- there has never been any direct evidence that viruses can injure human vessels. Now, thanks to a surprising discovery at Washington University School of Medicine in St. Louis, there is a new reason to reconsider the idea. In a recent issue of Nature Medicine, the researchers reported that a virus related to those that cause mononucleosis and Kaposi's sarcoma can injure arteries in mice, the first time such an effect had been seen in mammals. The study was supported by Monsanto-Searle, the National Institutes of Health and the National Cancer Institute.

"We're still a long way from showing that viruses can trigger atherosclerosis or other vascular diseases in humans," says senior author Herbert W. Virgin, M.D., Ph.D., an assistant professor of pathology, molecular microbiology and medicine. "But now we have a better idea that it may be possible, and we know which viruses might be involved."

The discovery at the School of Medicine echoes recent studies that suggest a link between bacterial infections and some vascular diseases. That link is still inconclusive, but Virgin believes it's entirely possible that both viruses and bacteria might be capable of damaging blood vessels and triggering disease. "It's highly unlikely that one single agent is the cause of all vascular disease," he says.

If viruses do in fact set the stage for atherosclerosis, physicians may someday be able to prevent the dise
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Contact: Linda Sage
sage@medicine.wustl.edu
314-286-0119
Washington University in St. Louis
1-Mar-1998