Hajjar D P
Department of Biochemistry, Cornell University Medical College, New York, NY 10021.
Am J Pathol. 1991 Dec;139(6):1195-211.
Human atherogenesis is a pleiotropic process with an undefined cause. Several pathologic factors have been linked to the disease process, including arterial injury or activation of the endothelium, which may injury or activation of the endothelium, which may initiate proatherosclerotic events in the vessel wall. Atherosclerotic lesions are characterized, in part, by the presence of activated immune cells, abnormal cell proliferation, and altered cholesterol metabolism. These activated immunocompetent cells in plaques produce vasoactive mediators that can alter homeostasis and may promote the arteriopathy. Both molecular and structural evidence is presented that herpesviruses, by way of induction of altered gene function and cellular cholesterol metabolism, coupled with their ability to activate coagulation and a monocyte receptor on the infected endothelium, are involved in major pathogenic events associated with atherosclerosis and thrombosis. Work from the author's laboratory, as well as from other research groups, have shown that avian and human herpesviruses act specifically to induce alterations to the surface and inner layers of the blood vessel wall that may predispose to atherosclerosis and its attendant clinical complications.
人类动脉粥样硬化形成是一个病因不明的多效性过程。多种病理因素与该疾病进程相关，包括动脉损伤或内皮激活，这可能引发血管壁中的促动脉粥样硬化事件。动脉粥样硬化病变部分特征在于存在活化的免疫细胞、异常细胞增殖和胆固醇代谢改变。斑块中的这些活化免疫活性细胞产生血管活性介质，可改变体内平衡并可能促进动脉病变。有分子和结构证据表明，疱疹病毒通过诱导基因功能改变和细胞胆固醇代谢，再加上其激活凝血和感染内皮细胞上单核细胞受体的能力，参与了与动脉粥样硬化和血栓形成相关的主要致病事件。作者实验室以及其他研究小组的研究表明，禽类和人类疱疹病毒可特异性地诱导血管壁表层和内层发生改变，这些改变可能易引发动脉粥样硬化及其相关临床并发症。
