Exploring the mechanism of comorbidity in patients with T1DM and COVID-19: Integrating bioinformatics and Mendelian randomization methods

During the coronavirus disease 2019 (COVID-19) pandemic, the incidence of type 1 diabetes mellitus (T1DM) has increased. Additionally, evidence suggests that individuals with diabetes mellitus may have increased susceptibility to severe acute respiratory syndrome coronavirus 2 infection. However, the specific causal relationships and interaction mechanisms between T1DM and COVID-19 remain unclear. This study aims to investigate the causal relationship between T1DM and COVID-19, utilizing differential gene expression and Mendelian randomization analyses. Differentially expressed gene sets from datasets GSE156035 and GSE171110 were intersected to identify shared genes, analyzed for functional enrichment. Mendelian randomization models were employed to assess causal effects, revealing no direct causal link between T1DM and COVID-19 in the European population (P > .05). Notably, DNA replication and sister chromatid cohesion 1 (DSCC1) showed negative causal associations with both diseases (T1DM: OR = 0.943, 95% CI: 0.898-0.991, P = .020; COVID-19: OR = 0.919, 95% CI: 0.882-0.958, P < .001), suggesting a protective effect against their comorbidity. This genetic evidence highlights DSCC1 as a potential target for monitoring and managing the co-occurrence of T1DM and COVID-19.