Enteroviruses are believed to trigger or accelerate islet autoimmunity in genetically susceptible individuals, thereby resulting in loss of functional insulin-producing β-cells and type 1 diabetes mellitus (T1DM). Although enteroviruses are primarily involved in acute and lytic infections in vitro and in vivo, they can also establish a persistent infection. Prospective epidemiological studies have strongly associated the persistence of enteroviruses, especially coxsackievirus B (CVB), with the appearance of islet autoantibodies and an increased risk of T1DM. CVB can persist in pancreatic ductal and β-cells, which leads to structural or functional alterations of these cells, and to a chronic inflammatory response that promotes recruitment and activation of pre-existing autoreactive T cells and β-cell autoimmune destruction. CVB persistence in other sites, such as the intestine, blood cells and thymus, has been described; these sites could serve as a reservoir for infection or reinfection of the pancreas, and this persistence could have a role in the disturbance of tolerance to β-cells. This Review addresses the involvement of persistent enterovirus infection in triggering islet autoimmunity and T1DM, as well as current strategies to control enterovirus infections for preventing or reducing the risk of T1DM onset.

肠道病毒被认为会触发或加速遗传易感个体的胰岛自身免疫，从而导致功能性产生胰岛素的 β 细胞和 1 型糖尿病 (T1DM) 丧失。尽管肠道病毒主要参与体外和体内的急性和溶解性感染，但它们也可以建立持续性感染。前瞻性流行病学研究表明，肠道病毒，尤其是柯萨奇病毒 B (CVB) 的持续存在与胰岛自身抗体的出现和 T1DM 风险增加密切相关。CVB 可以持续存在于胰腺导管和 β 细胞中，从而导致这些细胞的结构或功能改变，并导致慢性炎症反应，促进预先存在的自身反应性 T 细胞的募集和激活以及 β 细胞自身免疫性破坏。已经描述了 CVB 在其他部位的持续存在，例如肠道、血细胞和胸腺；这些部位可以作为胰腺感染或再感染的宿主，这种持久性可能在干扰对 β 细胞的耐受性中起作用。本综述讨论了持续性肠道病毒感染在触发胰岛自身免疫和 T1DM 中的作用，以及当前控制肠道病毒感染以预防或降低 T1DM 发病风险的策略。