巨细胞病毒感染和动脉粥样硬化

许多临床和实验研究表明巨细胞病毒感染能够引起动脉硬化，但巨细胞病毒感染如何引起动脉硬化的具体机理尚未十分清楚。本综述具体讨论了巨细胞病毒感染和动脉硬化的关联性以及具体机理。研究表明，巨细胞病毒基因和病毒粒子入侵血管细胞，刺激血管上皮细胞释放炎性细胞因子，从而破换血管上皮细胞以及血管壁，导致血管增生，血管增生的病变导致动脉硬化。自我免疫在巨细胞病毒感染期间的变化也会刺激淋巴细胞游离到血管壁，从而促进动脉硬化的发生。另一个途径是巨细胞病毒和Toll样受体相互作用，从而刺激炎性细胞因子的释放，导致动脉硬化。但需要更多研究来进一步说明巨细胞病毒感染和动脉硬化之间的关联机理以及在临床上的应用。

CMV infection and atherosclerosis

There is a wealth of clinical and experimental evidence indicating the interaction of CMV infection and atherosclerosis. However, the mechanism by which CMV infection is implicated in atherosclerosis is still unclear. This review discusses the association between CMV infection and atherosclerosis, and recent studies about the mechanisms involved in. Initial results show that CMV infection causes the initial injury to the vascular endothelium and vascular wall, which triggers an angiogenesis. The possible mechanism is that expression of CMV genes and virons induces the production of inflammatory cytokines in vascular cells, which may contribute to the acceleration of atherosclerosis. Autoimmunity maybe be involved in promoting atherosclerosis during CMV infection by migration of T cells into the arterial wall. Finally, the alternative mechanism is that the interaction between CMV and TLR promotes the production of inflammatory cytokines and ultimately contributes to the acceleration of atherosclerosis. More mechanisms involved in virus-mediated acceleration of atherosclerosis are needed to be unraveled and used in clinics.