Do pathogens accelerate atherosclerosis?

Infection with the pathogens human cytomegalovirus (HCMV) or Chlamydia pneu monia (CP) is linked to the development of vascular disease, including athe rosclerosis. The role of pathogens in vasculopathies has been controversial . However, animal models have demonstrated a direct link between infection with CP and herpesviruses and the development of vascular disease. Clinical studies have shown a direct association of HCMV and CIP with the accelerat ion of vascular disease. This article will review the evidence supporting t he role for CP and HCMV in the development of vascular disease and will sug gest a potential mechanism for HCMV acceleration of the disease process. Va scular diseases are the result of either mechanical or immune-related injur y followed by inflammation and subsequent smooth muscle cell (SMC) prolifer ation and/or migration from the vessel media to the intima, which culminate s in vessel narrowing. A number of in vitro and in vivo models have provide d potential mechanisms involved in pathogen-mediated vascular disease. Rece ntly, we have demonstrated that HCMV infection of arterial but not venous S MC results in significant cellular migration in vitro. Migration was depend ent on expression of the HCMV-encoded chemokine receptors, US28, and the pr esence of the chemokines, RANTES or MCP-1. Migration involved chemotaxis an d provided the first evidence that viruses may induce migration of SMC towa rd sites of chemokine production through the expression of a virally encode d chemokine receptor in infected SMC. Because SMC migration into the neoint imal space is the hallmark of vascular disease, these observations provide a molecular link between HCMV and the development of vascular disease.