{"title":"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","authors":"D. Alber, P. Vallance, K. Powell","doi":"10.1161/01.ATV.0000016046.94521.68","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":8418,"journal":{"name":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2002-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"14","resultStr":"{\"title\":\"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\",\"authors\":\"D. Alber, P. Vallance, K. Powell\",\"doi\":\"10.1161/01.ATV.0000016046.94521.68\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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.\",\"PeriodicalId\":8418,\"journal\":{\"name\":\"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2002-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"14\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1161/01.ATV.0000016046.94521.68\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1161/01.ATV.0000016046.94521.68","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.