Liu Lei, Tuo Hou-Zhen, Wang Rui-Jin, Yi Li, Wang Jia-Wei, Wang De-Xin
Department of Neurology, Beijing Friendship Hospital, Capital Medical University, China.
Neurol Res. 2011 Jun;33(5):473-81. doi: 10.1179/016164111X13007856084007.
Past exposure to human cytomegalovirus has been suggested to participate in the pathogenetic events associated with atherosclerotic lesion establishment and progression. However, whether ongoing human cytomegalovirus infection is related to plaque instability, and subsequent acute cerebral ischemia, is relatively unknown. The purpose of this study was to evaluate the potential relationships between active human cytomegalovirus infection and ischemic stroke, especially in regard to metabolism and inflammation.
Ninety-nine acute ischemic stroke patients, associated with large artery atherosclerosis, were divided into two groups based on the presence or absence of human cytomegalovirus immunoglobulin M (IgM) (human cytomegalovirus-IgM-positive/human cytomegalovirus-IgM-negative = 33:66). Baseline clinical characteristics, inflammatory factors, and biochemical assessments were compared in both groups. Then, all patients and human cytomegalovirus-IgM-positive patients were divided into quartiles according to their high-sensitivity C-reactive protein levels, respectively, and risk factors were compared. Finally, correlations between inflammatory factors (high-sensitivity C-reactive protein and white blood cell count) and other atherosclerosis risk factors in both human cytomegalovirus-IgM-positive and -negative subjects were evaluated.
An association between human cytomegalovirus-IgM seropositivity and atherogenic modification of metabolism and inflammatory status were not found in this study. Both age and white blood cell count increased across quartiles of high-sensitivity C-reactive protein in all subjects (P = 0.001), while age and low-density lipoprotein cholesterol increased across quartiles of high-sensitivity C-reactive protein in the human cytomegalovirus-IgM-positive group (P = 0.02 and 0.007, respectively). Multivariate linear regression analysis showed that high-sensitivity C-reactive protein was associated with age in human cytomegalovirus-IgM-positive group (P = 0.002), while no other factor was associated with white blood cell count in these subjects.
Our study provided no evidence for the direct implication of active systemic human cytomegalovirus infection, represented by human cytomegalovirus-IgM positivity, in the pathogenesis of acute ischemic strokes, particularly those involving plaque instability and metabolic disorders.
既往接触过人巨细胞病毒被认为参与了与动脉粥样硬化病变形成和进展相关的致病过程。然而，目前人巨细胞病毒持续感染是否与斑块不稳定及随后的急性脑缺血相关，相对尚不明确。本研究的目的是评估活动性人巨细胞病毒感染与缺血性卒中之间的潜在关系，尤其是在代谢和炎症方面。
99例与大动脉粥样硬化相关的急性缺血性卒中患者，根据人巨细胞病毒免疫球蛋白M（IgM）的有无分为两组（人巨细胞病毒-IgM阳性/人巨细胞病毒-IgM阴性 = 33:66）。比较两组的基线临床特征、炎症因子和生化指标。然后，所有患者及人巨细胞病毒-IgM阳性患者分别根据其高敏C反应蛋白水平分为四分位数，并比较危险因素。最后，评估人巨细胞病毒-IgM阳性和阴性受试者中炎症因子（高敏C反应蛋白和白细胞计数）与其他动脉粥样硬化危险因素之间的相关性。
本研究未发现人巨细胞病毒-IgM血清阳性与代谢和炎症状态的致动脉粥样硬化改变之间存在关联。在所有受试者中，随着高敏C反应蛋白四分位数的增加，年龄和白细胞计数均升高（P = 0.001），而在人巨细胞病毒-IgM阳性组中，随着高敏C反应蛋白四分位数的增加，年龄和低密度脂蛋白胆固醇升高（分别为P = 0.02和0.007）。多变量线性回归分析显示，在人巨细胞病毒-IgM阳性组中，高敏C反应蛋白与年龄相关（P = 0.002），而在这些受试者中，没有其他因素与白细胞计数相关。
我们的研究没有提供证据表明以人巨细胞病毒-IgM阳性为代表的活动性全身性人巨细胞病毒感染直接参与急性缺血性卒中的发病机制，尤其是那些涉及斑块不稳定和代谢紊乱的卒中。
