Melnick J L, Adam E, Debakey M E
Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 77030.
Eur Heart J. 1993 Dec;14 Suppl K:30-8.
An avian herpesvirus is known to cause atherosclerosis in chickens. The same virus can induce a proliferative disease, malignant lymphoma, suggesting that this agent may also have transforming potential and thus stimulate the proliferation of arterial smooth muscle cells, a prominent feature of atherogenesis. The evidence for involvement of cytomegalovirus (CMV), a member of the human herpesvirus family, in atherosclerosis is much more circumstantial. The finding of CMV antigen and nucleic acid sequences in arterial smooth muscle cells of humans suggests that viral infection of the arterial wall may be common in the general population, including patients with severe atherosclerosis. In seroepidemiological studies, high levels of CMV antibodies were found to be associated with clinically manifest atherosclerotic disease, suggesting that a periodically activated latent infection or a continuously active infection is present in patients with atherosclerosis. Since the viral genome but not infectious virus is found in arterial cells, the artery itself may be the site of CMV latency. Of particular significance is the recent finding that heart transplant recipients, who are immunosuppressed, and who are also actively infected with CMV, are prone to develop accelerated atherosclerosis in the transplanted organ. Although suggestive, these observations by themselves do not demonstrate that viruses have a role in the pathogenesis of atherosclerosis, but they support a working hypothesis of the steps involved.
已知一种禽疱疹病毒可导致鸡患动脉粥样硬化。同一病毒能诱发一种增殖性疾病——恶性淋巴瘤，这表明该病原体可能也具有转化潜能，从而刺激动脉平滑肌细胞增殖，而这是动脉粥样硬化形成的一个显著特征。人疱疹病毒家族成员巨细胞病毒（CMV）参与动脉粥样硬化的证据则更为间接。在人类动脉平滑肌细胞中发现CMV抗原和核酸序列，这表明动脉壁的病毒感染在普通人群中可能很常见，包括患有严重动脉粥样硬化的患者。在血清流行病学研究中，发现高水平的CMV抗体与临床显性动脉粥样硬化疾病相关，这表明动脉粥样硬化患者存在周期性激活的潜伏感染或持续活跃的感染。由于在动脉细胞中发现的是病毒基因组而非感染性病毒，动脉本身可能是CMV潜伏的部位。特别重要的是最近的一项发现，即接受心脏移植的患者，他们免疫功能低下且同时被CMV积极感染，在移植器官中容易出现加速的动脉粥样硬化。尽管这些观察结果具有启发性，但它们本身并不能证明病毒在动脉粥样硬化发病机制中起作用，但它们支持了所涉及步骤的一个工作假设。
