All About Multiple Sclerosis

More MS news articles for April 2004

Epstein-Barr Virus in Pediatric Multiple Sclerosis

http://www.medscape.com/viewarticle/474614?src=search

April, 2004
Source: Alotaibi S, Kennedy J, Tellier R, Stephens D, Banwell B; JAMA. 2004;291(15):1875-1879
Carolyn Brockington, MD
Medscape Journal Scan

Overview

Multiple sclerosis (MS) is an inflammatory disorder involving the central nervous system white matter and is characterized by multifocal areas of demyelination, loss of oligodendrocytes, and astrogliosis with relative preservation of axons. The exact cause of the disease is unclear but likely encompasses a variety of mechanisms, including autoimmunity, infection, bystander demyelination, and heredity. Although the exact role of viral infections in the initiation and maintenance of MS is unknown, several viruses, including Epstein-Barr virus (EBV), have been shown to cause demyelination. It appears there must be a window of immunologic vulnerability in childhood when exposure to a putative infectious agent initiates a chain of events that results in the development of the disease. If the theory is true and EBV infection is involved in the initiation of MS, then children with MS should demonstrate serologic evidence of prior EBV exposure at the time of their MS diagnosis and at an age when the majority of their healthy peers have yet to be exposed to the virus. Alotaibi and colleagues conducted a case-control study of viral samples to evaluate whether children with MS are more likely to be seropositive for EBV or other common viruses than their healthy, age-matched peers.

Results

Viral samples were collected (from March 1994 to February 2003) from 30 pediatric MS patients, 90 emergency department controls matched 3:1 with the MS patients by year of birth, and 53 healthy control children. The archived serum samples were analyzed for the presence of immunoglobulin G antibodies directed against EBV viral capsid antigens, nuclear antigens, and early antigens; cytomegalovirus; parvovirus B19; herpes simplex virus; and varicella zoster. The mean time from the first MS attack to viral sample acquisition was 1.36 years. None of the MS children were receiving MS-targeted therapies at the time of sample acquisition, although now many have been given treatment. The results of the study demonstrated pediatric MS patients were significantly more likely to have experienced EBV infection than their peers. Serologic evidence for remote EBV infection was present in 83% of pediatric MS patients as compared with 42% of emergency department and healthy controls (P < .001). Of interest pediatric MS patients were less likely than controls to have been exposed to herpes simplex virus (P = .003), whereas seropositivity for cytomegalovirus, parvovirus B19, and varicella zoster did not differ between MS patients and controls. Of note, 5 pediatric MS patients were negative for all 3 EBV antigens.

Comment

Although the results of the study suggested an association between EBV infection and pediatric MS, it is clear that further research is needed to uncover its exact role in the development of MS. Because EBV is not the only virus implicated in MS and evidently not a requisite trigger (as evidenced by the 5 EBV-negative pediatric MS patients), the pathogenesis of MS must be influenced by a variety of factors, including immune responses to various environmental agents ( such as viruses encountered during the pediatric window of immunologic vulnerability).
 

Copyright © 2004, Medscape