Type 1 diabetes (T1D) is an autoimmune disease resulting from the combined effects of genetic and environmental factors. In recent years, respiratory viral infections have been regarded as important environmental triggers for T1D. This article provides a systematic review of the epidemiological associations, potential mechanisms, and prevention and treatment strategies related to respiratory viral infections and the onset of T1D. Multiple large-scale international cohort studies have shown that respiratory viral infections, such as influenza virus, SARS-CoV-2, and human coronavirus, can significantly increase the risk of T1D, particularly ingenetically susceptible  children. Mechanistically, viruses can promote disease progression through two pathways: direct infection of beta cells (via ACE2-dependent invasion and necroptosis) and indirect activation of autoimmunity (via molecular mimicry, bystander activation, and interferon-mediated insulin resistance). In addition, factors such as gut-lung axis dysregulation, host genetic background, and timing of exposure can further modulate the risk of T1D. Clinically, T1D associated with respiratory viral infections often presents with acute onset and a high incidence of diabetic ketoacidosis. Targeted prevention and control strategies include vaccination of high-risk populations, early viral surveillance, blood glucose management during infection, and immunomodulatory therapy. Future efforts should strengthen population-based studies to elucidate virus-specific pathogenic mechanisms and establish a T1D prevention and control system based on environmental monitoring.