Early childhood CMV infection may decelerate the progression to clinical type 1 diabetes

• Published in: Pediatric diabetes Vol. 20; no. 1; pp. 73 - 77
• Main Authors: Ekman, Ilse, Vuorinen, Tytti, Knip, Mikael, Veijola, Riitta, Toppari, Jorma, Hyöty, Heikki, Kinnunen, Tuure, Ilonen, Jorma, Lempainen, Johanna
• Format: Journal Article
• Language: English
• Published: Former Munksgaard John Wiley & Sons A/S 01.02.2019; Wiley Subscription Services, Inc
• Subjects: Antigens; Autoantibodies; Autoimmunity; Children; CMV; Cytomegalovirus; Diabetes; Diabetes mellitus; Diabetes mellitus (insulin dependent); Genotypes; Glutamate decarboxylase; Glutamic acid; Histocompatibility antigen HLA; Immunoglobulin G; Infections; Insulin; Insulinoma; Survival analysis; type 1 diabetes; type 1 diabetes; cytomegalovirus; CMV; autoantibodies
• ISSN: 1399-543X; 1399-5448
• DOI: 10.1111/pedi.12788

Aims/Hypothesis Evidence of the role of cytomegalovirus (CMV) infection in the pathogenesis of type 1 diabetes (T1D) has remained inconclusive. Our aim was to elucidate the possible role of CMV infection in the initiation of islet autoimmunity and in the progression to clinical T1D among children with human leukocyte antigen (HLA)‐conferred T1D risk. Methods A total of 1402 children from the prospective Type 1 Diabetes Prediction and Prevention (DIPP) study were analyzed for CMV‐specific IgG antibodies during early childhood. All the children carried HLA‐DQ genotypes associated with increased risk for T1D. The effect of CMV infection on the appearance of T1D‐associated autoantibodies (insulin autoantibodies [IAA], glutamic acid decarboxylase [GADA], and insulinoma antigen‐2 [IA‐2A], n = 356) and on the progression rate to clinical T1D (n = 233) were analyzed with Kaplan‐Meier survival analysis and Log‐rank test. Results Early childhood CMV infection was inversely associated with the development of T1D during childhood. Cumulative progression to T1D was decreased in subjects with an early CMV infection (P = 0.035). In further analyses, the effect of early CMV infection on the initiation of islet autoimmunity and progression to clinical T1D were examined separately. Interestingly, early CMV infection did not affect the appearance of T1D‐associated autoantibodies but a decelerating effect was observed on the progression rate from islet autoimmunity to clinical T1D (P = 0.015). Conclusion Our results suggest that an early childhood CMV infection may decelerate the progression from islet autoimmunity to clinical T1D among at‐risk children and may thus protect these children from progressing to T1D during childhood.