Fabricant C G, Hajjar D P, Minick C R, Fabricant J
Am J Pathol. 1981 Nov;105(2):176-84.
In our previous experiments, atherosclerosis similar to that in humans was reproducibly induced in both normocholesterolemic and hypercholesterolemic specific-pathogen-free (SPF) chickens by infection with Marek's disease herpesvirus (MDV). In contrast, uninfected chickens fed either relatively cholesterol-poor or cholesterol-supplemented diets did not develop this arterial disease. In experiments reported here, the hypothesis that infection of arterial smooth muscle cells (SMCs) with MDV would enhance lipid accumulation in these cells was tested. The number of MDV-infected SMCs with lipid stained with oil red O was assessed, and the lipid content of these cells was quantitated chemically by chromatographic and fluorometric analyses. These data were compared to those of uninfected control cells and, in the case of chemical analyses, were also compared to SMCs infected with a second avian herpesvirus, turkey herpesvirus (HVT). Results indicate the following: 1) The percentage of MDV-infected SMCs containing stainable lipid was significantly greater than the percentage of uninfected SMCs; 2) Increased total lipid accumulation was observed in MDV-infected SMC, particularly cholesterol (CH) and cholesteryl esters (CEs), as compared with uninfected or HVT-infected cells; 3) The types of CEs and nonesterified fatty acids (NEFA) accumulating in MDV-infected cells (particularly saturated types of CEs and NEFAs) were significantly different than those in uninfected or HVT-infected SMCs. These qualitative and quantitative differences in lipid content between infected and uninfected SMCs suggest that infection with MDV results in altered intracellular lipid metabolism. Results support the hypothesis that lipid accumulation in arteries of normocholesterolemic chickens may result from MDV infection acting at the cellular level to induce lipid accumulation that resembles that in human atheroarteriosclerosis.
在我们之前的实验中，通过感染马立克氏病疱疹病毒（MDV），在正常胆固醇水平和高胆固醇水平的无特定病原体（SPF）鸡中均可重复诱导出类似于人类的动脉粥样硬化。相比之下，喂食相对低胆固醇或高胆固醇饮食的未感染鸡并未发生这种动脉疾病。在本文报道的实验中，测试了MDV感染动脉平滑肌细胞（SMC）会增强这些细胞中脂质积累的假设。评估了用油红O染色的含脂质的MDV感染SMC的数量，并通过色谱和荧光分析对这些细胞的脂质含量进行化学定量。将这些数据与未感染的对照细胞的数据进行比较，并且在化学分析的情况下，还与感染了另一种禽疱疹病毒——火鸡疱疹病毒（HVT）的SMC进行比较。结果表明：1）含有可染色脂质的MDV感染SMC的百分比显著高于未感染SMC的百分比；2）与未感染或HVT感染的细胞相比，在MDV感染的SMC中观察到总脂质积累增加，尤其是胆固醇（CH）和胆固醇酯（CEs）；3）在MDV感染的细胞中积累的CEs和非酯化脂肪酸（NEFA）的类型（特别是饱和类型的CEs和NEFAs）与未感染或HVT感染的SMC中的显著不同。感染和未感染的SMC之间脂质含量的这些定性和定量差异表明，MDV感染导致细胞内脂质代谢改变。结果支持这样的假设，即正常胆固醇水平鸡的动脉中脂质积累可能是由于MDV感染在细胞水平上起作用，诱导出类似于人类动脉粥样硬化的脂质积累。
