Yoon J W
Julia McFarlane Diabetes Research Centre, Faculty of Medicine, University of Calgary, Alberta, Canada.
Ann Med. 1991 Oct;23(4):437-45. doi: 10.3109/07853899109148087.
Insulin-dependent diabetes mellitus (IDDM), also known as type I diabetes, results from the destruction of pancreatic beta cells. During the past few decades, genetic factors, autoimmunity and viral infections have been extensively studied as the possible cause of beta cell destruction. The evidence for virus-induced diabetes comes largely from experiments in animals, but several studies in humans also point to viruses as a trigger of this disease in some cases. There are at least two possible mechanisms for the involvement of viruses in the pathogenesis of IDDM: (a) cytolytic infection of beta cells may result in destruction of the cells without the induction of autoimmunity, or may be a final insult leading to the clinical onset of diabetes in individuals with an already decreased beta cell mass resulting from an autoimmune process; and (b) persistent viral infection (e.g. retrovirus, rubella virus, cytomegalovirus) may result in the triggering of autoimmune IDDM in certain circumstances. Regarding the latter possibility, viruses may insert, expose, or alter antigens in the plasma membrane of the beta cell, which may initiate autoimmunity leading to the destruction of the cells.
胰岛素依赖型糖尿病（IDDM），也称为I型糖尿病，是由胰腺β细胞的破坏引起的。在过去几十年中，遗传因素、自身免疫和病毒感染作为β细胞破坏的可能原因受到了广泛研究。病毒诱导糖尿病的证据主要来自动物实验，但一些人体研究也表明，在某些情况下病毒是这种疾病的触发因素。病毒参与IDDM发病机制至少有两种可能的机制：（a）β细胞的溶细胞性感染可能导致细胞破坏而不诱导自身免疫，或者可能是一种最终损伤，导致因自身免疫过程导致β细胞数量已经减少的个体发生糖尿病临床发作；（b）持续性病毒感染（如逆转录病毒、风疹病毒、巨细胞病毒）在某些情况下可能导致自身免疫性IDDM的触发。关于后一种可能性，病毒可能插入、暴露或改变β细胞质膜中的抗原，这可能引发自身免疫，导致细胞破坏。
