Viral Infection Might Trigger High Blood Pressure

May 15 (HealthDay News) -- A hidden viral infection that most adults harbor could be a cause of high blood pressure, animal studies indicate.

Mice infected with cytomegalovirus (CMV) were more likely to develop not only high blood pressure but also the hardening of the arteries called atherosclerosis, according to a report in the May 15 issue of PLoS Pathogens by researchers at Beth Israel Deaconess Hospital in Boston.

"This could be of immense importance," said lead researcher Dr. Clyde Crumpacker, a professor of medicine at Harvard Medical School and an investigator in the Division of Infectious Diseases at Beth Israel Deaconess. "The implication for the human population is that antiviral therapy or a vaccine could be an intervention for high blood pressure."

CMV infection is widespread, Crumpacker noted. Studies indicate that between 60 percent and 99 percent of adults worldwide are infected, according to the study. But aside from pregnancy, where CMV infection is associated with serious birth defects, it causes no problems for most adults "until they get something that compromises the immune system," he noted.

"Vascular [blood vessel] injury has been suspected for quite a while," Crumpacker said. "What we have added, in collaboration with cardiologists, is evidence that in mice, CMV can cause an increase in blood pressure."

Blood vessel problems related to CMV infection were first noted in heart transplant recipients, Crumpacker said. Those who were CMV-positive were more likely to have blockage of the heart arteries.

The new study brought together specialists from several fields, including cardiology, virology and pathology to look at the phenomenon in mice. The study included four groups of mice, two fed a standard diet, and two fed a high-cholesterol diet. After four weeks, mice in one standard-diet group and one high-cholesterol group were infected with CMV.

"We were able to measure blood pressure directly in the arteries of the mice," Crumpacker said. The studies showed increased blood pressure in the infected mice after six weeks, but not in the uninfected group. It also showed that 30 percent of the infected mice in the high-cholesterol group developed atherosclerosis as well as high blood pressure.

There are several possible mechanisms for the pressure-raising effect of CMV, Crumpacker said. One is that it increases the activity of renin, an enzyme associated with high blood pressure. The study showed that CMV also increases activity of angiotensin 11, a protein involved in high blood pressure.

Most cases of high blood pressure in humans are of unknown origin, Crumpacker said. "Ninety-eight percent of the time, we don't know what the cause is," he said. If CMV infection is established as a cause -- something that requires much more research -- the way would be open for better methods of prevention and treatment, Crumpacker said.

"This is very exciting and important work," said Dr. Mark R. Schleiss, who holds the American Legion chair of pediatric infectious disease at the University of Minnesota and is a leading figure in the drive to develop a CMV vaccine.

"It is virtually certain that cytomegalovirus infection makes at least some contribution to cardiovascular disease in people," Schleiss said. "Obviously, cytomegalovirus is not the whole picture. There are other issues, including smoking, physical activity and diet. But this extends our body of knowledge about the role cytomegalovirus infection can play, and it is an important role, in cardiovascular disease."

The effort to develop a CMV vaccine has concentrated on childbirth, since infection during pregnancy is the leading cause of mental retardation and deafness in children, Schleiss said. "Now there is an urgency to develop a vaccine for men as well as women," he said.


SOURCES: Clyde Crumpacker, M.D., professor, medicine, Harvard Medical School, and investigator, Division of Infectious Diseases, Beth Israel Deaconess Hospital, Boston; Mark R. Schleiss, M.D., American Legion chair of pediatric infectious disease, University of Minnesota, Minneapolis; May 15, 2009, PLoS Pathogens

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