More MS news articles for Dec 2001

EBV Infection Temporally Linked to Multiple Sclerosis

NEW YORK (Reuters Health) Dec 25 - Infection with Epstein-Barr virus (EBV) has been associated with the risk of multiple sclerosis (MS). Now, a prospective study published in the December 26th issue of The Journal of the American Medical Association provides temporal evidence that the relationship may be causal.

Dr. Alberto Ascherio, from the Harvard School of Public Health in Boston, and colleagues studied 144 women with definite or probable MS and 288 healthy age-matched controls. Blood samples from both groups were analyzed for antibodies to specific EBV and cytomegalovirus (CMV) antigens.

The researchers identified 18 women with MS who had their blood collected before disease onset. Antibody levels to several EBV antigens were significantly higher in these women than in their matched controls. In fact, a four-fold increase in antibody titers to EBNA-2, a nuclear antigen, was associated with a nearly four-fold increased risk of MS. In contrast, anti-CMV antibody levels were not predictive of MS.

Among the 126 women with MS whose blood was collected after disease onset, significant but generally weaker elevations in anti-EBV antibody levels were noted compared with their matched controls.

The current findings indicate that significant elevations in anti-EBV antibody titers are present before MS onset. However, because EBV infection is very common and MS relatively rare, other cofactors certainly play a role. "Final proof of causality could come from the demonstration that a suitable [EBV] vaccine prevents MS," the authors note.

In a related editorial, Dr. Donald H. Gilden, from the University of Colorado in Denver, comments that "while the findings would suggest a role of EBV in the etiology of MS, cerebrospinal fluid (CSF) data would be helpful, since the IgG in MS patients' brain tissue and CSF is synthesized intrathecally and may more accurately reflect the immune response at the site of disease."

JAMA 2001;286:3083-3088,3127-3129.

Copyright © 2001 Reuters Ltd