Capron L
Service de médecine interne et pathologie vasculaire, hôpital Broussais, Paris.
Rev Prat. 1990 Oct 21;40(24):2227-33.
Our understanding of the pathogenesis and aetiology of atherosclerosis remains incomplete. An infection by herpesviruses is among the plausible hypotheses. In chicken, inoculation with Marek's disease virus provokes arterial lesions closely resembling atherosclerotic plaques. Experiments done on cultured arterial cells have shown that herpesviruses might enhance atherogenesis. Herpesviruses molecules (proteins, messenger ribonucleic acid, deoxyribonucleic acid) are commonly found in the human arterial wall. According to a recent study using gene amplification by the polymerase chain reaction, the complete cytomegalovirus genome can be detected in 90 p. 100 of the samples from atherosclerotic plaques and in 53 p. 100 of the samples from normal arterial wall. Cytomegalovirus infection appears to increase the risk and severity of atherosclerotic lesions which develop in heart grafts and compromise their survival. These data are not sufficient to prove that herpesviruses, especially cytomegalovirus, play a causal role in human atherosclerosis. The viral hypothesis, however, must be considered as serious and is certainly worth further investigations.
我们对动脉粥样硬化发病机制和病因的理解仍不完整。疱疹病毒感染是众多合理假说之一。在鸡身上,接种马立克氏病病毒会引发与动脉粥样硬化斑块极为相似的动脉病变。对培养的动脉细胞进行的实验表明,疱疹病毒可能会促进动脉粥样硬化的发生。疱疹病毒分子(蛋白质、信使核糖核酸、脱氧核糖核酸)在人类动脉壁中普遍存在。根据最近一项使用聚合酶链反应进行基因扩增的研究,在90%的动脉粥样硬化斑块样本和53%的正常动脉壁样本中可检测到完整的巨细胞病毒基因组。巨细胞病毒感染似乎会增加心脏移植中发生的动脉粥样硬化病变的风险和严重程度,并危及移植心脏的存活。这些数据不足以证明疱疹病毒,尤其是巨细胞病毒,在人类动脉粥样硬化中起因果作用。然而,病毒假说必须被视为一个严肃的问题,当然值得进一步研究。