颈动脉硬化患者HCMV感染与血清Lp(a)、ApoA1、ApoB、ApoB/ApoA1浓度的关系

目的通过研究颈动脉硬化患者人类巨细胞病毒(HCMV)感染状态与脂蛋白a(Lp(a))、载脂蛋白A1(ApoA1)、载脂蛋白B(ApoB)及ApoB/ApoA1比值的关系,探讨HCMV致动脉硬化的机制。方法利用实时荧光定量PCR技术检测研究对象外周血白细胞中HCMV DNA拷贝数,并利用ELISA技术检测血清中HCMV IgM,同时利用生化分析技术检测Lp(a)、ApoA1、ApoB含量并计算ApoB/ApoA1比值。结果在颈动脉硬化阳性组中,HCMV阳性率为54.7%(35/64),对照组HCMV阳性率为25.0%(5/20),差异有统计学意义(P<0.05);颈动脉硬化阳性组中的Lp(a)、ApoB及ApoB/ApoA1比值均显著高于颈动脉硬化阴性组(0.46±0.31 vs 0.30±0.24,0.77±0.22 vs 0.66±0.18,0.62±0.21 vs 0.51±0.17,P均<0.05),颈动脉硬化阳性组中的ApoA1明显低于颈动脉硬化阴性组(1.35±0.42 vs 1.58±0.41,P<0.05)。在颈动脉硬化阴性组中,HCMV阳性者及HCMV阴性者其ApoA1及ApoB含量差异无统计学意义(1.56±0.44 vs 1.66±0.34,0.67±0.21 vs 0.64±0.10,P均>0.05)。在颈动脉硬化阳性组中,HCMV阳性者血清ApoA1含量明显低于HCMV阴性者(1.27±0.33 vs 1.46±0.34,P<0.05),而ApoB在HCMV阳性者及阴性者中差异无统计学意义(0.78±0.19 vs 0.76±0.15,P>0.05);不论颈动脉硬化阳性组还是对照组,HCMV阳性者的Lp(a)及ApoB/ApoA1比值均显著高于HCMV阴性者(0.59±0.20 vs 0.29±0.17,0.67±0.21 vs 0.56±0.17,0.54±0.36 vs 0.23±0.12,0.58±0.16 vs 0.40±0.14,P均<0.05)。结论 HCMV感染可能通过改变宿主脂类代谢引起或促进动脉硬化的发病过程。

Correlation of HCMV Infection with the Concentrations of Lp(a), ApoA1, ApoB and ApoB/ApoA1 Ratio in Patients with Carotid Atherosclerosis

Objective To explore the relationship between human cytomegalovirus（HCMV） infection and the serum concentrations of Lp（a）,ApoA1,ApoB and ApoB/ApoA1 ratio,so as to clarify the mechanisms of arteriosclerosis induced by HCMV.Methods The research objects were classified into carotid atherosclerosis positive group and carotid atherosclerosis negative group（control group） according to ultrasonography diagnosis.HCMV DNA copies in the peripheral blood leukocytes were detected by real-time PCR and HCMV IgM in sera were detected by enzyme-linked immunosorbent assay（ELISA）.The concentrations of Lp（a）,ApoA1,ApoB in sera were measured by biochemical techniques,and ApoB/ApoA1 ratio was calculated.Results The positive rate of HCMV in the carotid atherosclerosis positive group（54.7%,35/64） was significantly higher than that in the control group（25.0%,5/20）（P0.05）.So were the serum concentrations of Lp（a）,ApoB and ApoB/ApoA1 ratio（0.46±0.31 vs 0.30±0.24,0.77±0.22 vs 0.66±0.18,0.62±0.21 vs 0.51±0.17,respectively,all P0.05）.However,the serum concentration of ApoA1 in patients with carotid atherosclerosis was lower than that in the controls（1.35±0.42 vs 1.58±0.41,P0.05）.In the control group,the serum concentrations of ApoA1 and ApoB did not indicate any significant difference between patients with HCMV infection and without HCMV infection（1.56±0.44 vs 1.66±0.34,0.67±0.21 vs 0.64±0.10,respectively,both P0.05）.However,in the carotid atherosclerosis positive group,the serum concentration of ApoA1 in patients with HCMV infection was significantly lower than that in those without HCMV infection（1.27±0.33 vs 1.46±0.34,P0.05）,while no significant difference was found for serum ApoB concentration（0.78±0.19 vs 0.76±0.15,P0.05）.Regardless of with or without carotid atherosclerosis,the serum concentration of Lp（a） and the ApoB/ApoA1 ratio were statistically higher in patients with HCMV infection than those in patients without HCMV infection（0.59±0.20 vs 0.29±0.17,0.67±0.21 vs 0.56±0.17 in patients with carotid atherosclerosis,0.54±0.36 vs 0.23±0.12,0.58±0.16 vs 0.40±0.14 in patients without carotid atherosclerosis,respectively,all P0.05）.Conclusions Human cytomegalovirus infection may trigger or promote the pathologic processes of atherosclerosis by modifying host lipid metabolism.