JDRF, 26 Broadway, 14th Floor, New York, NY, 10004, USA.
Institute of Biomedical and Clinical Science, University of Exeter Medical School, RILD Building, Barrack Road, Exeter, EX2 5DW, UK.
Diabetologia. 2019 May;62(5):744-753. doi: 10.1007/s00125-019-4811-7. Epub 2019 Jan 23.
In type 1 diabetes, pancreatic beta cells are destroyed by chronic autoimmune responses. The disease develops in genetically susceptible individuals, but a role for environmental factors has been postulated. Viral infections have long been considered as candidates for environmental triggers but, given the lack of evidence for an acute, widespread, cytopathic effect in the pancreas in type 1 diabetes or for a closely related temporal association of diabetes onset with such infections, a role for viruses in type 1 diabetes remains unproven. Moreover, viruses have rarely been isolated from the pancreas of individuals with type 1 diabetes, mainly (but not solely) due to the inaccessibility of the organ. Here, we review past and recent literature to evaluate the proposals that chronic, recurrent and, possibly, persistent enteroviral infections occur in pancreatic beta cells in type 1 diabetes. We also explore whether these infections may be sustained by different virus strains over time and whether multiple viral hits can occur during the natural history of type 1 diabetes. We emphasise that only a minority of beta cells appear to be infected at any given time and that enteroviruses may become replication defective, which could explain why they have been isolated from the pancreas only rarely. We argue that enteroviral infection of beta cells largely depends on the host innate and adaptive immune responses, including innate responses mounted by beta cells. Thus, we propose that viruses could play a role in type 1 diabetes on multiple levels, including in the triggering and chronic stimulation of autoimmunity and in the generation of inflammation and the promotion of beta cell dysfunction and stress, each of which might then contribute to autoimmunity, as part of a vicious circle. We conclude that studies into the effects of vaccinations and/or antiviral drugs (some of which are currently on-going) is the only means by which the role of viruses in type 1 diabetes can be finally proven or disproven.
在 1 型糖尿病中,胰腺β细胞被慢性自身免疫反应破坏。该疾病发生在遗传易感个体中,但环境因素的作用已被提出。病毒感染长期以来一直被认为是环境触发因素的候选者,但由于缺乏 1 型糖尿病中胰腺急性、广泛、细胞病变效应的证据,也缺乏糖尿病发病与此类感染密切相关的时间关联证据,因此病毒在 1 型糖尿病中的作用仍未得到证实。此外,由于器官不可及,病毒很少从 1 型糖尿病个体的胰腺中分离出来,主要(但并非唯一)是由于器官不可及。在这里,我们回顾了过去和最近的文献,以评估慢性、复发性、可能持续性肠道病毒感染发生在 1 型糖尿病中胰腺β细胞的假说。我们还探讨了这些感染是否可能随着时间的推移由不同的病毒株持续存在,以及在 1 型糖尿病的自然史中是否可能发生多次病毒攻击。我们强调,在任何给定时间,只有少数β细胞似乎被感染,而肠道病毒可能会失去复制能力,这可以解释为什么它们很少从胰腺中分离出来。我们认为,肠道病毒感染β细胞在很大程度上取决于宿主先天和适应性免疫反应,包括β细胞引发的先天反应。因此,我们提出病毒可以在多个层面上在 1 型糖尿病中发挥作用,包括在自身免疫的触发和慢性刺激、炎症的产生以及β细胞功能障碍和应激的促进,其中每一个都可能作为一个恶性循环的一部分,导致自身免疫。我们得出结论,对疫苗接种和/或抗病毒药物(其中一些正在进行中)的研究是最终证明或否定病毒在 1 型糖尿病中作用的唯一方法。