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Reovirus Delays Diabetes Onset but Does Not Prevent Insulitis in Nonobese Diabetic Mice

机译:呼肠孤病毒可延缓糖尿病的发作但不能预防非肥胖型糖尿病小鼠的胰岛炎

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摘要

Mice infected with reovirus develop abnormalities in glucose homeostasis. Reovirus strain type 3 Abney (T3A) was capable of systemic infection of nonobese diabetic (NOD) mice, an experimental model of autoimmune diabetes. Reovirus antigen was detected in pancreatic islets of T3A-infected mice, and primary cultures of pancreatic islets from NOD mice supported T3A growth. Significantly fewer T3A-infected animals compared to uninfected controls developed diabetes. However, despite the alteration in diabetes penetrance, insulitis was evident in T3A-infected mice. These results suggest that viral infection of NOD mice alters autoimmune responses to β-cell antigens and thereby delays development of diabetes.
机译:呼肠孤病毒感染的小鼠体内葡萄糖体内稳态异常。呼肠孤病毒3型Abney(T3A)株能够全身感染非肥胖糖尿病(NOD)小鼠,这是自身免疫性糖尿病的实验模型。在感染T3A的小鼠的胰岛中检测到呼肠孤病毒抗原,来自NOD小鼠的胰岛的原代培养物支持T3A的生长。与未感染的对照组相比,感染T3A的动物明显减少。然而,尽管糖尿病外表能力发生了改变,但在感染了T3A的小鼠中仍存在明显的胰岛炎。这些结果表明,NOD小鼠的病毒感染会改变对β细胞抗原的自身免疫反应,从而延迟糖尿病的发展。

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