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Cardiovascular Research 1998 38(1):237-246; doi:10.1016/S0008-6363(97)00315-5
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Atherosclerosis in Marek's disease virus infected hypercholesterolemic roosters is reduced by HMGCoA reductase and ACE inhibitor therapy

Alexandra Lucasa,*,1, Erbin Daia,1, Li-Ying Liua,1 and Patric N Nationb

aDivision of Cardiology, John P. Robarts Research Institute, Box 5015, 100 Perth Drive, University of Western Ontario, London, Ontario, Canada, N6A-5K8
bDepartment of Lab Animal Services, University of Alberta, Edmonton, Alberta, Canada

* Corresponding author. Tel.: +1 (519) 6633214/4071; fax: +1 (519) 6633789; e-mail: arl@rri.uwo.ca

Objective: Accelerated atherosclerosis is associated with herpesviral infection both in transplant patients and after balloon angioplasty. Marek's disease virus (MDV) is a herpesvirus that induces accelerated atherosclerosis associated with the development of an invasive lymphoma in hyperlipemic roosters. We have examined the effects of pravastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA) reductase inhibitor and quinapril, an angiotensin converting enzyme (ACE) inhibitor, on atherosclerosis development in MDV infected, cholesterol fed rooster chicks. Methods: The effects of these drugs on plaque growth after MDV infection were examined in two studies. In Study 1, MDV infected White Leghorn rooster chicks were divided into 4 groups assigned to normal or high cholesterol diet, and treated at three months of age with either pravastatin or saline. In Study 2, cholesterol fed rooster chicks infected with MDV were divided into 3 groups for treatment with either pravastatin, quinapril, or saline control. Results: A significant decrease in plaque area was detected after 60 days of treatment with both pravastatin and quinapril in cholesterol fed chicks (P<0.001). Lymphocyte infiltration into the arterial wall or target organs was not inhibited by treatment with either drug. Conclusions: (1) HMGCoA reductase inhibitor and ACE inhibitor therapy reduce atherosclerosis induced by virus infection and cholesterol diet, but this decrease in plaque growth is not due to a reduction in lymphocyte invasion. (2) MDV infection in cholesterol fed roosters provides a model for virus-induced arterial injury in atherogenesis.

KEYWORDS Marek's disease virus; Atherosclerosis; Angiotensin converting enzyme inhibitor; HMGCoA reductase inhibitor; White Leghorn roosters; Lymphocyte

1 Department of Medicine, University of Alberta, Edmonton, Alberta (Institution at which this work was performed).


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