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(Circulation. 1996;94:2694-2695.)
© 1996 American Heart Association, Inc.

Articles

Can a Viral Serine Proteinase Inhibitor Prevent Postangioplasty Restenosis?

Edgar Haber, MD

the Center for the Prevention of Cardiovascular Disease, Harvard School of Public Health and Harvard Medical School, Boston, Mass.

Correspondence to Dr Edgar Haber, Harvard School of Public Health, 655 Huntington Ave, Boston, MA 02115-6018. E-mail haber@cvlab.harvard.edu.

Key Words: Editorials • viruses • immune system • enzymes • stenosis

	Introduction

 
The sudden disappearance of the rabbit overpopulation in Australia was caused by the rapid spread of infection by the myxoma virus. Because it is transmitted venereally, the virus takes full advantage of the fabled promiscuity of its host. More importantly, however, it promotes secretion of a number of proteins that defeat the rabbit's cellular and immune responses to infection, thereby allowing the virus to take unopposed hold of its victim's tissues.

In this issue, Lucas et al¹ present evidence that the serine proteinase inhibitor SERP-1, which is encoded by the myxoma virus² and is essential to its ability to infect, ameliorates atherosclerosis in a rabbit model. Long ascribed to an inflammatory response, atherosclerosis begins with the transepithelial migration of monocytes and T cells from the blood to the neointimal space.³ Some of these monocytes then become macrophages that appear on histological examination as lipid-laden foam cells, which predominate in the earliest mass lesion of atherosclerosis, the fatty streak.³ The other clinically important forms of arteriosclerosis—postangioplasty restenosis, vein bypass graft failure, and transplant arteriosclerosis—can also begin as inflammatory lesions. All forms of arteriosclerosis are ultimately sustained by more complex processes that also involve migration of smooth muscle cells.

Lucas et al¹ obtained SERP-1 from tissue culture cells that had been infected with a recombinant vaccinia virus that also encoded SERP-1. They also obtained a mutant form of SERP-1 that lacked proteinase inhibitor activity, an important control. When native SERP-1 was infused locally (through a perforated catheter) at low doses or systemically . . . [Full Text of this Article]