Abstract：
Type 1 diabetes (T1D), a severe disease requiring intensive insulin treatment, carries an increased risk for complications and reduced lifespan. Certain viruses have been implicated in T1D\'s etiology, with \'live\', replicating enteroviruses (EVs) recently found in the pancreas at diagnosis. This discovery prompted a trial to slow down disease progression using antiviral drugs. A 6-month treatment combining pleconaril and ribavirin in new-onset T1D patients preserved residual insulin production after 1 year, unlike placebo. The results support the theory that viruses may cause T1D in genetically susceptible individuals. A low-grade, persistent viral infection may initiate a cascade of pathogenic mechanisms initially involving the innate immune system, inducing β-cell stress and neoantigen release, leading to autoimmunity, and eventually the destruction of insulin-producing β-cells.
摘要：
1型糖尿病（T1D），需要强化胰岛素治疗的严重疾病，会增加并发症的风险并缩短寿命。某些病毒与T1D的病因学有关，与\'活\'，最近在诊断时在胰腺中发现的复制型肠道病毒（EV）。这一发现促使一项使用抗病毒药物减缓疾病进展的试验。在新发病的T1D患者中，联合pleconaril和利巴韦林的6个月治疗保留了1年后的残余胰岛素产量。不像安慰剂.结果支持病毒可能在遗传易感个体中引起T1D的理论。一个低级的，持续性病毒感染可能会引发一系列最初涉及先天免疫系统的致病机制，诱导β细胞应激和新抗原释放，导致自身免疫,最终破坏产生胰岛素的β细胞。
