缺乏ISG15 E1酶UbE1L的小鼠对适应小鼠和非适应小鼠的乙型流感病毒感染的易感性增加。
Mice lacking the ISG15 E1 enzyme UbE1L demonstrate increased susceptibility to both mouse-adapted and non-mouse-adapted influenza B virus infection.
作者信息
Lai Caroline, Struckhoff Jessica J, Schneider Jana, Martinez-Sobrido Luis, Wolff Thorsten, García-Sastre Adolfo, Zhang Dong-Er, Lenschow Deborah J
机构信息
Department of Internal Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA.
出版信息
J Virol. 2009 Jan;83(2):1147-51. doi: 10.1128/JVI.00105-08. Epub 2008 Nov 12.
Abstract
ISG15 functions as a critical antiviral molecule against influenza virus, with infection inducing both the conjugation of ISG15 to target proteins and production of free ISG15. Here, we report that mice lacking the ISG15 E1 enzyme UbE1L fail to form ISG15 conjugates. Both UbE1L(-/-) and ISG15(-/-) mice display increased susceptibility to influenza B virus infection, including non-mouse-adapted strains. Finally, we demonstrate that ISG15 controls influenza B virus infection through its action within radioresistant stromal cells and not bone marrow-derived cells. Thus, the conjugation of ISG15 to target proteins within stromal cells is critical to its activity against influenza virus.
摘要
ISG15作为一种针对流感病毒的关键抗病毒分子发挥作用，感染会诱导ISG15与靶蛋白结合以及游离ISG15的产生。在此，我们报告缺乏ISG15 E1酶UbE1L的小鼠无法形成ISG15缀合物。UbE1L(-/-)小鼠和ISG15(-/-)小鼠对乙型流感病毒感染（包括非小鼠适应性毒株）均表现出易感性增加。最后，我们证明ISG15通过其在抗辐射基质细胞而非骨髓来源细胞中的作用来控制乙型流感病毒感染。因此，ISG15与基质细胞内靶蛋白的结合对其抗流感病毒活性至关重要。
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