Murine gamma-herpesvirus 68 causes severe large-vessel arteritis in mice lacking interferon-gamma responsiveness: a new model for virus-induced vascular disease.
Murine gamma-herpesvirus 68 causes severe large-vessel arteritis in mice lacking interferon-gamma responsiveness: a new model for virus-induced vascular disease.
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鼠伽马疱疹病毒 68 在缺乏干扰素伽马反应性的小鼠中引起严重的大血管动脉炎：病毒诱发的血管疾病的新模型。
DOI：
10.1038/nm1297-1346
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发表时间：
1997
期刊：
影响因子：
82.9
通讯作者：
Virgin,HW
中科院分区：
文献类型：
--
作者：
Weck,KE;DalCanto,AJ;Gould,JD;O'Guin,AK;Roth,KA;Saffitz,JE;Speck,SH;Virgin,HW
关于病毒对血管病理的可能贡献，以及免疫系统在调节这些过程中的作用，基本问题仍然没有解决。在这里，我们证明了小鼠感染γ疱疹病毒68(γHV68)为解决这些问题提供了一个新的模型。干扰素-γ受体缺陷(干扰素γR−/−)小鼠在γHV68感染后数周至数月死于严重的大血管全动脉炎。感染γHv68的B细胞缺陷和正常断奶小鼠表现出较轻的大血管动脉炎。免疫组织化学分析显示γHV68抗原存在于动脉病变中，并显示γHV68对平滑肌细胞有明显的趋向性。这些研究表明，干扰素-γ对于控制γHV68诱导的慢性血管病变是必不可少的，并提示γ-疱疹病毒是人类血管炎的候选病原体。
Fundamental issues remain unresolved regarding the possible contribution of viruses to vascular pathology, as well as the role of the immune system in regulating these processes. Here we demonstrate that infection of mice with γ-herpesvirus 68 (γHV68) provides a novel model for addressing these issues. Interferon-γ receptor-deficient (IFNγR−/−) mice died weeks to months after γHV68 infection from a severe large-vessel panarteritis. γHV68-infected B cell-deficient and normal weanling mice exhibited milder large-vessel arteritis. Immunohistochemical analyses demonstrated γHV68 antigen in arteritic lesions and revealed a striking tropism of γHV68 for smooth muscle cells. These studies demonstrate that IFN-γ is essential for control of chronic vascular pathology induced by γHV68 and suggest γ-herpesviruses as candidate etiologic agents for human vasculitis.