Could Delayed Primary Epstein-Barr Virus Infection Contribute to the Rising Incidence of Type 1 Diabetes?
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Type 1 diabetes mellitus (T1DM) incidence has been rising for several decades and varies markedly across countries, a pace and geographical spread that genetic susceptibility alone cannot explain, pointing to a major role for environmental factors. Viruses have long been regarded as triggers of islet autoimmunity, yet recent clinical and experimental observations suggest that Epstein-Barr virus (EBV) may instead exert immunoregulatory effects that could protect against islet autoimmunity. EBV establishes a lifelong infection in approximately 95% of adults worldwide in memory B cells, generally during the first years of life, but the age at primary infection has shifted progressively towards adolescence in high-income countries, reflecting improved hygiene standards. This review compares the age at primary EBV infection with T1DM incidence across regions and populations that differ in hygiene standards and cultural practices. Populations in which primary infection occurs in early childhood generally show a low incidence of T1DM and a high incidence of nasopharyngeal carcinoma (NPC), an EBV-induced cancer, whereas the opposite pattern is observed in some populations in which primary infection is delayed; comparable contrasts are found between ethnic groups living within the same country. Delayed exposure to EBV, a virus that has coevolved with the human lineage over millions of years and for which protective effects against islet autoimmunity have been proposed, may therefore contribute, alongside other environmental determinants, to the rising incidence of T1DM, potentially extending the 'Old friends' hypothesis to a common virus belonging to the Orthoherpesviridae family.