Enhanced atherogenesis is not an obligatory response to systemic herpesvirus infection in the ApoE-deficient mouse -: Comparison of murine γ-herpesvirus-68 and herpes simplex virus-1

被引:12
作者
Alber, DG
Vallance, P
Powell, KL
机构
[1] UCL, Wolfson Inst Biomed Res, London WC1E 6BT, England
[2] UCL, Rayne Inst, BHF Labs, Ctr Clin Pharmacol & Therapeut, London WC1E 6BT, England
关键词
atherosclerosis; infection; herpesvirus; animal models;
D O I
10.1161/01.ATV.0000016046.94521.68
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Viral and bacterial infectious agents have been implicated in the etiology of atherosclerosis. We have previously shown that a gamma-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 gamma-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.
引用
收藏
页码:793 / 798
页数:6
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