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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
Summary
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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