Herpes Virus Infection May Be One Cause Of Heart Disease With PM-Balloon Treatment Bjt
DALLAS (AP) _ A finding that the fever-blister virus may cause changes in artery walls is the latest to implicate herpes organisms in hardening of the arteries, a leading cause of heart attacks and strokes.
The new study described at the American Heart Association’s annual meeting found that the virus may aid formation of artery-clogging deposits, said David Hajjar of Cornell University Medical College in New York.
A series of studies have connected herpes viruses with hardening of the arteries, or atherosclerosis, which occurs when cholesterol and fats build up in the arteries, narrowing them and eventually cutting off the flow of blood.
The blockage can cause a heart attack if it occurs in an artery supplying the heart or a stroke in an artery supplying the brain. Heart attacks and strokes kill 700,000 Americans a year.
″Our hypothesis is that the virus early on transforms or alters cells within the blood vessel, so that during our years of development the blood vessel can’t handle all the cholesterol that comes in,″ Hajjar said Monday.
He said so-called smooth-muscle cells that lie in artery walls become unable to rid themselves of cholesterol after they have been infected with herpes simplex virus type 1, the virus that causes fever blisters.
″The cell becomes constipated,″ he said.
This does not mean that anyone who has fever blisters is at risk of atherosclerosis, Hajjar emphasized. Virtually the entire U.S. population has been exposed to herpes simplex type 1, and many do not develop atherosclerosis, which indicates that other factors play important roles in the disease process.
He said his finding, made on human smooth-muscle cells grown in the laboratory, does not suggest any new means of preventing or treating atherosclerosis.
It is theoretically possible that a herpes vaccine could reduce the risk of atherosclerosis, if such a vaccine were available, he said. But because herpes is only one cause of atherosclerosis, such a vaccine presumably would not eliminate the disease.
Hajjar’s study follows recent findings that herpes viruses are present in atherosclerotic deposits or ″plaques.″
Such findings have been reported by Earl Benditt of the University of Washington and Joseph Melnick of the Baylor College of Medicine in Houston.
Hajjar’s study focused on the smooth-muscle cells, which line blood vessel walls. He said that Douglas Cines of the University of Pennsylvania School of Medicine has recently found that herpes virus also damages the endothelium, or inner lining of arterial walls.
Cines found that when the endothelium is infected with herpes, it can suffer damage from the body’s immune system. That damage allows cholesterol into the vessel walls, where it accumulates in infected smooth-muscle cells that can not get rid of it, Hajjar said, offering a possible explanation of how herpes virus contributes to the disease.
Hajjar said that the herpes virus infection in smooth-muscle cells decreases the production of two enzymes the cells use to get rid of cholesterol.
He is now trying to determine whether other human herpes viruses produce the same effect in smooth-muscle cells, he said.