Indications that maternal coxsackie B virus infection during pregnancy is a risk factor for childhood-onset IDDM

G Dahlquist1, G Frisk, S A Ivarsson

  • 1Department of Pediatrics, Umeå University, Sweden.

Diabetologia
|November 1, 1995
PubMed

Insights

Mothers with coxsackie B virus type 3 (CBV-3) IgM antibodies at delivery had children with a higher risk of developing insulin-dependent diabetes (IDDM). This suggests a fetal infection may trigger autoimmune responses leading to beta-cell destruction.

Area of Science:

  • Virology
  • Immunology
  • Endocrinology

Background:

  • Childhood-onset insulin-dependent diabetes (IDDM) is a significant health concern.
  • The role of viral infections in the etiology of IDDM is under investigation.
  • Coxsackie B viruses (CBV) are suspected triggers for autoimmune diabetes.

Purpose of the Study:

  • To investigate the association between maternal IgM antibodies to coxsackie B virus (CBV) serotypes 2, 3, and 4 at delivery and the subsequent development of IDDM in their children.
  • To determine if specific CBV serotypes are linked to an increased risk of childhood IDDM.

Main Methods:

  • A population-based case-control study design was employed.
  • Serum samples from mothers of children with IDDM and matched control mothers were collected at the time of birth.
  • Sera were analyzed for IgM antibodies against CBV-2, CBV-3, and CBV-4 using radioimmunoassay.

Main Results:

  • A significantly higher frequency of CBV-3 IgM antibodies was found in mothers of children who later developed IDDM compared to control mothers.
  • The odds ratio for developing IDDM associated with CBV-3 IgM was 2.57 (95% CI: 1.02-7.31), indicating a 2.57-fold increased risk.
  • No significant association was found for CBV-2 or CBV-4 IgM antibodies.
  • The estimated etiological fraction for CBV-3 as a risk determinant was 27%.

Conclusions:

  • Maternal infection with CBV-3 during pregnancy may be a risk factor for childhood-onset IDDM.
  • Fetal infection with CBV could potentially initiate autoimmunity or lead to persistent infection, causing progressive beta-cell destruction.
  • Further research is warranted to elucidate the precise mechanisms linking CBV infection to IDDM pathogenesis.

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