Environmental factors, in particular viral infections, are thought to have an important role in the pathogenesis of type 1 diabetes mellitus (T1DM). The COVID-19 pandemic reinforced this hypothesis as many observational studies and meta-analyses reported a notable increase in the incidence of T1DM following infection with SARS-CoV-2 as well as an association between SARS-CoV-2 infection and the risk of new-onset T1DM. Experimental evidence suggests that human β-cells express SARS-CoV-2 receptors and that SARS-CoV-2 can infect and replicate in β-cells, resulting in structural or functional alterations of these cells. These alterations include reduced numbers of insulin-secreting granules, impaired pro-insulin (or insulin) secretion, and β-cell transdifferentiation or dedifferentiation. The inflammatory environment induced by local or systemic SARS-CoV-2 infection might result in a set of signals (such as pro-inflammatory cytokines) that lead to β-cell alteration or apoptosis or to a bystander activation of T cells and disruption of peripheral tolerance that triggers autoimmunity. Other mechanisms, such as viral persistence, molecular mimicry and activation of endogenous human retroviruses, are also likely to be involved in the pathogenesis of T1DM following SARS-CoV-2 infection. This Review addresses the issue of the involvement of SARS-CoV-2 infection in the development of T1DM using evidence from epidemiological, clinical and experimental studies.

环境因素，特别是病毒感染，被认为在 1 型糖尿病 (T1DM) 的发病机制中具有重要作用。 COVID-19 大流行强化了这一假设，因为许多观察性研究和荟萃分析报告称，感染 SARS-CoV-2 后 T1DM 的发病率显着增加，并且 SARS-CoV-2 感染与新冠肺炎风险之间存在关联。发病T1DM。实验证据表明，人类 β 细胞表达 SARS-CoV-2 受体，并且 SARS-CoV-2 可以感染 β 细胞并在 β 细胞中复制，导致这些细胞的结构或功能发生改变。这些改变包括胰岛素分泌颗粒数量减少、胰岛素原（或胰岛素）分泌受损以及β细胞转分化或去分化。局部或全身 SARS-CoV-2 感染引起的炎症环境可能会产生一系列信号（例如促炎细胞因子），导致 β 细胞改变或凋亡，或导致 T 细胞的旁观者激活和外周细胞的破坏。引发自身免疫的耐受性。其他机制，如病毒持久性、分子模拟和内源性人类逆转录病毒的激活，也可能参与 SARS-CoV-2 感染后 T1DM 的发病机制。本综述利用流行病学、临床和实验研究的证据，探讨了 SARS-CoV-2 感染与 T1DM 发展的关系。