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疱疹病毒诱导的鸡动脉粥样硬化

Herpesvirus-induced atherosclerosis in chickens.

作者信息

Fabricant C G, Fabricant J, Minick C R, Litrenta M M

出版信息

Fed Proc. 1983 May 15;42(8):2476-9.

PMID:6840298
Abstract

Repeated experiments have established that infection with Marek's disease herpesvirus (MDV) leads to atherosclerosis in specific pathogen free (SPF) normocholesterolemic chickens. Neither normocholesterolemic nor hypercholesterolemic uninfected SPF chickens develop this disease. The MDV-induced arterial disease is remarkably similar to chronic human atherosclerosis. Cholesterol and saturated cholesteryl esters accumulated in cultured arterial smooth muscle cells (SMC) infected with MDV. Similar preliminary observations were made in vivo. These findings suggest that MDV-induced alteration of SMC lipid metabolism is of major importance in the pathogenesis of MDV-induced atherosclerosis. In addition, immunization with turkey herpesvirus, used commercially to prevent MDV-induced tumors in chickens, also protected against MDV-induced atherosclerosis. This animal model has introduced important new dimensions and tools in atherosclerosis research: a defined etiologic agent (MDV) that causes atherosclerosis in a defined animal of known genetic susceptibility to the etiologic agent. With these tools, important mechanisms in the pathogenesis of atherosclerosis may be established in a relatively short period of time. Further, this animal model should be considered important in other models of atherosclerosis research because herpesvirus infections are ubiquitous in these animals. Finally, because humans are widely and persistently infected with up to five herpesviruses, these studies may lead to the understanding and eventual control of human atherosclerosis.

摘要

反复实验已证实,感染马立克氏病疱疹病毒(MDV)会导致特定病原体-free(SPF)正常胆固醇水平的鸡发生动脉粥样硬化。正常胆固醇水平或高胆固醇水平的未感染SPF鸡均不会患此病。MDV诱导的动脉疾病与人类慢性动脉粥样硬化极为相似。胆固醇和饱和胆固醇酯在感染MDV的培养动脉平滑肌细胞(SMC)中积累。在体内也有类似的初步观察结果。这些发现表明,MDV诱导的SMC脂质代谢改变在MDV诱导的动脉粥样硬化发病机制中至关重要。此外,用商业上用于预防鸡群中MDV诱导肿瘤的火鸡疱疹病毒进行免疫,也能预防MDV诱导的动脉粥样硬化。这种动物模型为动脉粥样硬化研究引入了重要的新维度和工具:一种明确的病原体(MDV),它能在对该病原体具有已知遗传易感性的特定动物中引发动脉粥样硬化。借助这些工具,可在相对较短的时间内确定动脉粥样硬化发病机制中的重要机制。此外,这种动物模型在其他动脉粥样硬化研究模型中也应被视为重要模型,因为疱疹病毒感染在这些动物中普遍存在。最后,由于人类广泛且持续感染多达五种疱疹病毒,这些研究可能会促成对人类动脉粥样硬化的理解并最终加以控制。

相似文献

1
Herpesvirus-induced atherosclerosis in chickens.疱疹病毒诱导的鸡动脉粥样硬化
Fed Proc. 1983 May 15;42(8):2476-9.
2
Herpesvirus infection enhances cholesterol and cholesteryl ester accumulation in cultured arterial smooth muscle cells.疱疹病毒感染会增强培养的动脉平滑肌细胞中胆固醇和胆固醇酯的积累。
Am J Pathol. 1981 Nov;105(2):176-84.
3
Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation.病毒诱导的动脉粥样硬化。疱疹病毒感染会改变主动脉胆固醇代谢和积聚。
Am J Pathol. 1986 Jan;122(1):62-70.
4
Marek's disease. XVII. Studies on virus induced-atherosclerosis.马立克氏病。十七。病毒诱导动脉粥样硬化的研究。
Virologie. 1987 Oct-Dec;38(4):245-50.
5
Atheroarteriosclerosis induced by infection with a herpesvirus.由疱疹病毒感染引起的动脉粥样硬化。
Am J Pathol. 1979 Sep;96(3):673-706.
6
Atherosclerosis induced by infection with Marek's disease herpesvirus in chickens.鸡感染马立克氏病疱疹病毒诱发动脉粥样硬化。
Am Heart J. 1999 Nov;138(5 Pt 2):S465-8. doi: 10.1016/s0002-8703(99)70276-0.
7
Intimal lipid accretion and elevated serum cholesterol in Marek's disease virus-inoculated chickens.接种马立克氏病病毒的鸡的内膜脂质积聚和血清胆固醇升高
Vet Pathol. 1996 Nov;33(6):704-8. doi: 10.1177/030098589603300611.
8
Partial inhibition by turkey herpesvirus of serotype 2 Marek's disease virus plaque formation and in vivo infectivity.火鸡疱疹病毒对2型马立克氏病病毒蚀斑形成和体内感染性的部分抑制作用。
Avian Dis. 1994 Oct-Dec;38(4):800-9.
9
Interaction of Marek's disease virus and Cryptosporidium baileyi in experimentally infected chickens.马立克氏病病毒与贝氏隐孢子虫在实验感染鸡中的相互作用。
Avian Dis. 2000 Oct-Dec;44(4):776-89.
10
Virus-induced atherosclerosis.病毒诱导的动脉粥样硬化。
J Exp Med. 1978 Jul 1;148(1):335-40. doi: 10.1084/jem.148.1.335.

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