ABSTRACT
Type 1 diabetes (T1D) is usually caused by immune-mediated destruction of islet beta-cells, and genetic and environmental factors are thought to trigger autoimmunity. Convincing evidence indicates that viruses are associated with T1D development and progression. During the coronavirus disease 2019(COVID-19) pandemic, cases of hyperglycemia, diabetic ketoacidosis (DKA), and new diabetes increased, suggesting that severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may be a trigger for or unmask T1D. Possible mechanisms of beta-cell damage include virus-triggered cell death, immune-mediated loss of pancreatic beta-cells, and damage to beta-cells due to infection of surrounding cells. This article examines the potential pathways by which SARS-CoV-2 affects islet beta-cells in the above three aspects. Specifically, we emphasize that T1D can be triggered by SARS-CoV-2 through several autoimmune mechanisms, including epitope spread, molecular mimicry and bystander activation. Given that the development of T1D is often a chronic, long-term process, it is difficult to currently draw firm conclusions as to whether SARS-CoV-2 causes T1D. This area needs to be focused on in terms of the long-term outcomes. More in-depth and comprehensive studies with larger cohorts of patients and long-term clinical follow-ups are required.