Modulation of vascular remodeling induced by a brief intraluminal exposure to the recombinant R7020 strain of Herpes simplex-1

Vascular proliferative disorders including restenosis after percutaneous intervention and de novo vein graft stenosis complicate up to 50% of procedures and are the leading cause of therapeutic failure. Vascular smooth muscle cell proliferation is believed to result from direct mechanical injury to the vessel, as well as in response to changes in the hemodynamic environment such as increased wall tension, decreased shear stress, or both. The purpose of the present experiment was to test the hypothesis that R7020, a more highly attenuated mutant of Herpes simplex virus-1 (HSV), would modulate the vascular remodeling response of fully circumferential vein grafts chronically exposed to low shear stress. Attenuated HSV may represent a novel therapeutic strategy for both the prevention and treatment of vascular proliferative disorders.