人类动脉细胞中的单纯疱疹病毒感染。对动脉粥样硬化的影响。
Herpes simplex virus infection in human arterial cells. Implications in arteriosclerosis.
作者信息
Hajjar D P, Pomerantz K B, Falcone D J, Weksler B B, Grant A J
机构信息
Department of Biochemistry, National Institutes of Health Specialized Center for Research in Thrombosis, Cornell University Medical College, New York, New York 10021.
出版信息
J Clin Invest. 1987 Nov;80(5):1317-21. doi: 10.1172/JCI113208.
Herpesviruses have been implicated as etiologic factors in the pathogenesis of human arteriosclerosis. We have examined the pathobiological effects of human herpes simplex virus (HSV-1) infection in influencing lipid accumulation and metabolism in human and bovine arterial smooth muscle cells (SMC). Significantly greater amounts of saturated cholesteryl esters (CE) and triacylglycerols (TG) accumulate in HSV-1-infected human and bovine arterial SMC than uninfected cells. This CE accumulation results, in part, from decreased CE hydrolysis. Furthermore, arachidonate-stimulated, HSV-1-infected arterial SMC have a reduced capacity to produce prostacyclin (an agonist of intracellular CE hydrolytic activity) than uninfected, stimulated SMC. It appears that HSV-1 may induce lipid accumulation in arterial SMC similar, in part, to the lipid accumulation observed in vivo during human atherogenesis. Thus, herpesviruses may contribute to lipid accumulation, which is a characteristic feature of atherosclerosis.
疱疹病毒被认为是人类动脉粥样硬化发病机制中的病因。我们研究了人类单纯疱疹病毒（HSV-1）感染对人和牛动脉平滑肌细胞（SMC）脂质积累和代谢的病理生物学影响。与未感染细胞相比，HSV-1感染的人和牛动脉SMC中积累了大量的饱和胆固醇酯（CE）和三酰甘油（TG）。这种CE积累部分是由于CE水解减少所致。此外，与未感染且受刺激的SMC相比，花生四烯酸刺激的HSV-1感染动脉SMC产生前列环素（细胞内CE水解活性的激动剂）的能力降低。看来，HSV-1可能在动脉SMC中诱导脂质积累，这在一定程度上类似于人类动脉粥样硬化形成过程中体内观察到的脂质积累。因此，疱疹病毒可能促成脂质积累，而脂质积累是动脉粥样硬化的一个特征。
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