TY - JOUR
T1 - Atherosclerosis in Marek's disease virus infected hypercholesterolemic roosters is reduced by HMGCoA reductase and ACE inhibitor therapy
AU - Lucas, Alexandra
AU - Dai, Erbin
AU - Liu, Li Ying
AU - Nation, Patric N.
N1 - Funding Information:
Alexandra Lucas is a Scientist at the Robart’s Research Institute and the Departments of Medicine and Microbiology and Immunology at the University of Western Ontario. This research was supported in part by a grant from the Alberta Heart and Stroke Foundation and a grant from Squibb Pharmaceuticals. Squibb and Park Davis supplied the drugs for testing in the MDV infected avian model. We would like to thank Marita Lundstrom Hobman and Dean Kolodziecjzyk for their help in proofing this manuscript. We would also like to thank Fran Plumb for helping with the typing of this manuscript.
PY - 1998/4
Y1 - 1998/4
N2 - 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 (HMGCoA) reductase inhibitor and quinapril, an angiotensin converting enzyme (ACE) inhibitor, on atherosclerosis development a 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 in 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.
AB - 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 (HMGCoA) reductase inhibitor and quinapril, an angiotensin converting enzyme (ACE) inhibitor, on atherosclerosis development a 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 in 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.
KW - Angiotensin converting enzyme inhibitor
KW - Atherosclerosis
KW - HMGCoA reductase inhibitor
KW - Lymphocyte
KW - Marek's disease virus
KW - White Leghorn roosters
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U2 - 10.1016/S0008-6363(97)00315-5
DO - 10.1016/S0008-6363(97)00315-5
M3 - Article
C2 - 9683927
AN - SCOPUS:0032051998
SN - 0008-6363
VL - 38
SP - 237
EP - 246
JO - Cardiovascular research
JF - Cardiovascular research
IS - 1
ER -