Human cytomegalovirus (hCMV) is a widespread member of the herpes family of viruses, with well over half of the world’s adult population thought to be infected. Most individuals are infected in early childhood and remain infected with latent virus for the rest of their lives. For the majority of people, infection is asymptomatic and usually undiagnosed but immunosuppression, caused by HIV-1 infection or drug therapy after transplant surgery, can lead to reactivation of the virus and overt infection. A number of studies have linked hCMV infection to cardiovascular disease, but the mechanisms underlying the pathology are not well understood. Writing in the May 15th edition of PLoS Pathogens, a team led by researchers at Beth Israel Deaconess Medical Center have now shown that infection with murine CMV (mCMV) leads to a significant increase in arterial pressure in mice. mCMV infection alone was sufficient to cause the observed increase in blood pressure. mCMV infection alone did not cause atherosclerosis in the aorta but, when combined with a high cholesterol diet, did cause classic plaque formation. The team went on to show that mCMV stimulated production of pro-inflammatory cytokines, IL6, TNF-α and MCP-1 which have previously been linked to high blood pressure. They also showed that mCMV infection induced renin expression in an infection dose-related manner in mouse renal cells and that hCMV induced a similar increase in human vascular endothelial cells. In mice, mCMV infection was additionally shown to lead to an increase in angiotensin II levels in serum and in tissue from the aorta.
Since the roles of renin and angiotensin II in hypertension are well established, the study provides a mechanism by which persistent CMV infection might increase blood pressure and also suggests that vaccination or antiviral therapy could have the potential to provide new treatments for cardiovascular disease.