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幼稚 HIV 感染者血液中的血小板激活因子及其基本代谢酶。

Platelet-activating factor and its basic metabolic enzymes in blood of naive HIV-infected patients.

机构信息

Department of Chemistry, National and Kapodistrian University of Athens, Greece.

出版信息

Angiology. 2012 Jul;63(5):343-52. doi: 10.1177/0003319711420608. Epub 2011 Sep 22.

DOI:10.1177/0003319711420608
PMID:21948973
Abstract

Platelet-activating factor (PAF), a mediator of proatherosclerotic inflammatory processes, is also implicated in endothelial dysfunction during human immunodeficiency virus (HIV) infection. We examined PAF metabolism in blood of naive male patients, 8 with early HIV infection (group A) and 17 just before treatment initiation (group B), versus 18 healthy age-matched males (group C). Statistical analysis was performed with 1-way analysis of variance (ANOVA) criterion and Pearson r test. Higher PAF biosynthesis in patients' leukocytes versus group C was accompanied by an increase in lipoprotein-associated phospholipase A2 (Lp-PLA2) activity that degrades PAF. Moreover, PAF synthesis was higher and Lp-PLA2 activity was lower in group B compared to group A. Lipoprotein-associated phospholipase A2 was positively correlated with viral load and negatively correlated with CD4 cell counts in group B. The activities of PAF-basic biosynthetic enzymes in patients' leukocytes were also negatively correlated with CD4 cell counts. The observed continuous increase in PAF biosynthesis during HIV infection progress seems to amplify the risk of AIDS manifestations and/or cardiovascular complications in HIV-infected patients, while a subsequent increase in Lp-PLA2 activity seems to be a host response.

摘要

血小板激活因子(PAF)是动脉粥样硬化炎症过程的中介物,也与人类免疫缺陷病毒(HIV)感染期间的内皮功能障碍有关。我们检查了 8 名早期 HIV 感染患者(A 组)和 17 名即将开始治疗的患者(B 组)以及 18 名年龄匹配的健康男性(C 组)的血液中 PAF 代谢情况。统计分析采用单因素方差分析(ANOVA)标准和 Pearson r 检验。与 C 组相比,患者白细胞中的 PAF 生物合成增加,伴随脂蛋白相关磷脂酶 A2(Lp-PLA2)活性升高,该酶可降解 PAF。此外,与 A 组相比,B 组的 PAF 合成更高,Lp-PLA2 活性更低。在 B 组中,Lp-PLA2 与病毒载量呈正相关,与 CD4 细胞计数呈负相关。患者白细胞中 PAF 基本生物合成酶的活性也与 CD4 细胞计数呈负相关。在 HIV 感染进展过程中观察到的 PAF 生物合成持续增加似乎会增加 HIV 感染患者出现艾滋病表现和/或心血管并发症的风险,而随后 Lp-PLA2 活性的增加似乎是宿主的反应。

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