Prevention of type 1 diabetes mellitus by the regulation of pancreas-specific retrovirus expression using the transplacental gene transfer method.

非肥胖糖尿病（NOD）小鼠发展为I型糖尿病，其特征在于大量淋巴细胞浸润到胰岛中。在这种类型的糖尿病的发病机制中，病毒的作用已被提出。我们在这里报告的逆转录病毒cDNA的表达被认为是特定的NOD小鼠胰腺的克隆。前病毒在序列上不同于所有其他已发表的C型逆转录病毒。该病毒具有相对较好保守的gag区和具有大缺失的截短的pol区。几乎所有的env区域都被删除，并且在pol区域的3 '端包括一个序列基序的痕迹。这些结构特征是复制缺陷病毒的特征。病毒mRNA表达水平在4周龄NOD小鼠中最高。胰岛炎的发作也发生在NOD小鼠的4周龄，因此表明病毒在该动物模型中的糖尿病发病机制中的作用。

The non-obese diabetic (NOD) mouse develop type I diabetes mellitus characterized by a massive lymphocytic infiltration into the pancreatic islets. A viral role has been suggested in the pathogenesis of this type of diabetes mellitus. We report here the cloning of retrovirus cDNA whose expression was considered to be specific to the pancreas of the NOD mouse. The provirus differs in sequence from all other published type C retrovirsues. The virus has a relatively well conserved gag region, and a truncated pol region with a large deletion. Almost all env region were deleted, and a trace of the sequence motif was included 3'to the pol region. These structural features are characteristic of replication defective viruses. Viral mRNA expression level was highest in 4-week-old NOD mice. The onset of insulitis also occurs from 4 weeks of age in the NOD mouse, thus suggesting a role for the virus in the pathogenesis of diabetes in this animal model.