自然杂志 ›› 2026, Vol. 48 ›› Issue (3): 190-196.doi: 10.3969/j.issn.0253-9608.2026.03.002

• 专题综述 • 上一篇    下一篇

呼吸道病毒:1型糖尿病的关键环境诱因

罗宽森,刘笑华,超晨,肖扬   

  1. 内分泌与代谢性疾病国家临床医学研究中心,糖尿病免疫学教育部重点实验室,中南大学湘雅二医院代谢内分泌科,长沙 410011
  • 收稿日期:2026-01-09 出版日期:2026-06-25 发布日期:2026-06-20
  • 基金资助:
    科技创新2030-“癌症、心脑血管、呼吸和代谢性疾病防治研究”重大项目(2023ZD0507300)

Respiratory viruses: a key environmental trigger for type 1 diabetes

LUO Kuansen, LIU Xiaohua, CHAO Chen, XIAO Yang   

  1. National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha 410011, China
  • Received:2026-01-09 Online:2026-06-25 Published:2026-06-20

摘要: 1型糖尿病(T1D)是遗传与环境因素共同作用的自身免疫性疾病,近年来呼吸道病毒感染被视为其重要的环境触发因素。本文系统综述了呼吸道病毒感染与T1D发病的流行病学关联、潜在机制及防治策略。多项国际大型队列研究表明,流感病毒、SARS-CoV-2及人冠状病毒等呼吸道病毒感染可显著增加T1D风险,尤其在遗传易感儿童中。机制上,病毒可通过直接感染β细胞(ACE2依赖性入侵、坏死性凋亡)和间接激活自身免疫(分子模拟、旁观者激活、干扰素介导的胰岛素抵抗)双重途径推动疾病进程。此外,肠道-呼吸道轴紊乱、宿主遗传背景及暴露时机等因素可进一步增加T1D患病风险。临床上,呼吸道病毒感染相关T1D常表现为急性起病、高糖尿病酮症酸中毒发生率。针对性的防控策略包括高危人群疫苗接种、早期病毒监测、感染期血糖管理及免疫调节治疗。未来需加强人群研究,明确病毒特异性致病机制,构建基于环境监测的T1D防控体系。

关键词: 1型糖尿病, 呼吸道病毒感染, 发病机制, 防治策略, 环境因素

Abstract: 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.