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Common viruses associated with lower pediatric multiple sclerosis risk

E Waubant1, E M Mowry, L Krupp

  • 1UCSF Regional Pediatric Multiple Sclerosis Center, 350 Parnassus Ave., Suite 908, San Francisco, CA 94117, USA. emmanuelle.waubant@ucsf.edu

Neurology
|June 8, 2011
PubMed
Abstract

Insights

Common viral infections like Epstein-Barr virus (EBV) may increase pediatric multiple sclerosis (MS) risk, while cytomegalovirus (CMV) might decrease it. Herpes simplex virus 1 (HSV-1) interactions with HLA-DRB1 influence MS susceptibility.

Area of Science:

  • Pediatric neurology
  • Immunology
  • Virology

Background:

  • Pediatric multiple sclerosis (MS) provides a model to study viral influences on disease risk.
  • Investigating common childhood viruses like Epstein-Barr virus (EBV), cytomegalovirus (CMV), and herpes simplex virus (HSV) in relation to MS susceptibility.
  • Examining the interplay between viral seroprevalence and specific Human Leukocyte Antigen (HLA) genotypes in pediatric MS.

Purpose of the Study:

  • To determine the association between seroprevalence of EBV, CMV, and HSV-1 and the risk of developing pediatric MS.
  • To investigate the potential modifying effect of HLA-DRB1*1501/1503 status on the relationship between viral infections and MS.
  • To explore interactions between viral infections and HLA genotypes in predicting pediatric MS risk.

Main Methods:

  • Retrospective analysis of prospectively collected data from pediatric MS patients and control groups.
  • Testing for seroprevalence of EBV, CMV, and HSV-1 in subjects up to 18 years of age.
  • Statistical analysis including multivariate models adjusted for demographic and genetic factors.

Main Results:

  • Epstein-Barr nuclear antigen-1 seropositivity was linked to a 3.78-fold increased odds of pediatric MS (p=0.004).
  • Cytomegalovirus infection was associated with a reduced risk of MS (OR 0.27, p=0.004).
  • A significant interaction between HSV-1 status and HLA-DRB1 alleles was observed, altering MS risk based on HLA-DRB1*15 status.

Conclusions:

  • Findings suggest certain common viral infections may paradoxically lower MS susceptibility.
  • The complex interplay between viruses, HLA genotypes, and MS risk warrants further investigation.
  • Elucidating the mechanisms behind these risk modifications is crucial for understanding MS pathogenesis.

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