强化动脉粥样硬化不是apoe缺陷小鼠对全身疱疹病毒感染的强制性反应:小鼠&ggr;-疱疹病毒-68和单纯疱疹病毒-1的比较

D. Alber, P. Vallance, K. Powell
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引用次数: 14

摘要

病毒和细菌感染因子与动脉粥样硬化的病因有关。我们之前已经证明,&ggr;-疱疹病毒可以加速载脂蛋白e缺陷(apoE−/−)小鼠的动脉粥样硬化。为了确定病毒诱导的全身免疫反应是否足以引发增强的动脉粥样硬化形成,我们用小鼠&ggr;-疱疹病毒-68 (MHV-68)或单纯疱疹病毒-1 (HSV-1)感染apoE−/−小鼠。在这项研究中,我们发现这两种病毒都能够在apoE−/−小鼠中诱导细胞介导和体液免疫反应,这种反应持续了24周。虽然鼻内或腹腔感染MHV-68可诱导apoE−/−小鼠血清中相似水平的病毒特异性IgG1和IgG2a抗体,但感染HSV-1的小鼠血清中抗HSV-1 IgG2a抗体水平高于IgG1抗体水平。此外,在hsv -1感染动物的主动脉中未检测到病毒信息,而我们之前已经证明,早在感染后5天就可以在感染小鼠的主动脉中检测到MHV-68 mRNA。与对照小鼠相比,感染MHV-68的apoE−/−小鼠显示动脉粥样硬化加速,而感染HSV-1的小鼠则没有。这些数据表明,对任何特定感染因子的全身免疫反应都不足以诱导apoE - / -小鼠动脉粥样硬化的增强,并指出特定的感染或免疫机制可能是病毒增强动脉粥样硬化发生所必需的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Enhanced Atherogenesis Is Not an Obligatory Response to Systemic Herpesvirus Infection in the ApoE-Deficient Mouse: Comparison of Murine &ggr;-Herpesvirus-68 and Herpes Simplex Virus-1
Viral and bacterial infectious agents have been implicated in the etiology of atherosclerosis. We have previously shown that a &ggr;-herpesvirus can accelerate atherosclerosis in the apolipoprotein E–deficient (apoE−/−) mouse. To address whether a virally induced systemic immune response is sufficient to trigger enhanced atheroma formation, we infected apoE−/− mice with murine &ggr;-herpesvirus-68 (MHV-68) or herpes simplex virus-1 (HSV-1). In this study, we show that both viruses were able to induce a cell-mediated and humoral immune response in the apoE−/− mouse, which was sustained over a period of 24 weeks. Although intranasal or intraperitoneal infection with MHV-68 induced similar levels of virus-specific IgG1 and IgG2a antibodies in the serum of apoE−/− mice, those infected with HSV-1 showed higher anti–HSV-1 IgG2a compared with IgG1 antibody levels. In addition, viral message was not detected in the aortas of HSV-1–infected animals, whereas we have shown previously that MHV-68 mRNA can be detected in the aortas of infected mice as early as 5 days after infection. Compared with control mice, apoE−/− mice infected with MHV-68 showed accelerated atherosclerosis, whereas mice infected with HSV-1 did not. These data indicate that a systemic immune response to any particular infectious agent is insufficient to induce enhanced atherosclerosis in the apoE−/− mouse and point to specific infections or immune mechanisms that might be essential for virally enhanced atherogenesis.
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