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Progress in Research > Research Highlights Summer/Fall 2006

The Complex Link between Infection and MS

By Sara Bernstein

It would be simple if multiple sclerosis were caused by an infectious agent, such as a bacterium – an antibiotic might cure the disease. Although infectious triggers have been associated with MS, none has been found to cause the disease. Because evidence suggests that MS may occur years, even decades after a triggering event, the study of infectious agents in MS is actually quite complicated, necessitating several approaches.

Studying People and Infections

Studying who gets MS and their experience with infections — a specialty of epidemiologists — is one approach. Recently, Gerald N. DeLorenze, PhD (Kaiser Permanente Division of Research) and colleagues reported that individuals with significant exposure to Epstein-Barr virus (EBV), which causes infectious mononucleosis, were twice as likely to develop MS up to 20 years later (Archives of Neurology, June 2006). The study, funded by a pilot grant from the National MS Society, adds to evidence linking EBV to the risk of developing MS, but does not prove that EBV causes MS.

Alvaro Alonso, PhD and colleagues (Harvard School of Public Health) investigated a role in MS for the bacterium Chlamydophila pneumoniae. With funding from a Society pilot grant, the team identified
163 individuals with MS from a database of British patients who were followed for at least three years before MS onset. People treated with antibiotics for exposure to this bacterium did not have an increased risk of MS. Interestingly, increased risk was identified among those taking penicillin, possibly implicating another trigger (American Journal of Epidemiology, June 1, 2006).

William A. Sibley, MD (University of Arizona, Tucson) was honored for groundbreaking epidemiological efforts with the National MS Society/American Academy of Neurology’s 2006 John Dystel Prize for MS

Research. In 1985, Sibley and colleagues were first to report that during the weeks before and after viral infections, annual MS relapse rates in individuals were almost threefold greater than other times (Lancet, June 1985). This study, confirmed by others, shows that MS relapses can be triggered by infections. It does not prove, however, that MS originates with an infection.

It would take carefully controlled studies of thousands of people to confirm an agent as a cause of MS. The Society recently launched a task force to investigate the feasibility of establishing such studies.

Does the Response Trigger MS?

Because of the variety of agents with possible links to MS, some researchers suggest that the immune response to such agents (rather than the agents themselves) may trigger the attack on myelin and underlying nerve fibers in MS. In one mouse model of MS, symptoms are induced by Theiler’s murine encephalomyelitis virus (TMEV). TMEV infects macrophages (a scavenger cell that ingests and destroys foreign substances such as bacteria, viruses, and cell debris), which produce messenger proteins that spur on MS-like disease. Some mice, however, resist TMEV-induced symptoms. Thomas Petro, PhD (University of Nebraska Medical Center, Omaha/Lincoln) is investigating why, with Society funding.

Petro’s team has found that a “transcription factor” that activates genes, called IRF-3, is pre-activated in macrophages from mice susceptible to TMEV. This sets off a cascade of molecular events resulting in elevated production of a subunit of IL-23, an inflammatory messenger that contributes to MS. (These results are in press at the Journal of Virology.) Interestingly, studies searching for MS susceptibility genes in people have found that one MS gene may be located in the same region as the gene for IRF-3.

Stanley Perlman, MD, PhD (University of Iowa, Iowa City) is investigating a model in which MS-like damage is caused by mouse hepatitis virus (MHV), with Society funding. Perlman’s team has shown that a mouse strain that lacks the necessary B and T cells to generate a rigorous immune response does not develop MS-like disease in response to MHV unless cells are “added in” from normal mice.

Perlman is now investigating how these immune cells induce damage. Results indicate the importance of the immune messenger interferon gamma, and, in some instances, a molecule on T cells called NKG2D; disabling these molecules decreased MHV damage (Journal of Virology, August 2005).

These studies suggest that genetic or immune factors may enhance susceptibility to a variety of infectious triggers.

Sleeping Triggers

Other researchers suspect that the immune attack in MS may be triggered by a virus that lies dormant in the nervous system until reactivated years after infection. Ralph Feuer, PhD (The Scripps Research Institute, La Jolla, CA) is investigating coxsackievirus (CV), which causes myelin damage after infection in children. Dr. Feuer’s studies suggest that CV may lie dormant within mouse cells after infection and can be reactivated if the cells change.

Feuer, a Society-funded fellow, is applying CV to samples of brain cells in laboratory dishes, to identify which cells are damaged by the infection. He recently showed that CV targets immature nerve cells; infected cells lose the ability to multiply (The Journal of Neuroscience, March 2, 2005). Whether or not CV is eventually linked to MS, these experiments demonstrate how a common, dormant infection may
play a role in MS.

Myelin Mimics

Still another hypothesis is that an infection may trigger MS or MS relapses through “molecular mimicry.” In this scenario, because of structural similarities between myelin and viral/bacterial proteins, immune cells generated against the invader also attack the body’s own myelin. Stephen D. Miller, PhD (Northwestern University, Chicago) and colleagues have developed a model of MS-like disease induced by molecular mimicry, with funding from the Society (Journal of Clinical Investigation, July 2001). They injected mice with a virus that was fused to part of a bacterial gene that is similar to a myelin gene. The mice quickly developed myelin damage and paralysis, caused by a T-cell attack on myelin.

Miller’s team recently showed that injecting mice with a myelin protein segment resembling a virus worsened previously existing disease (Journal of Virology, July 2005). His studies shed light on how molecular mimicry may contribute to MS and MS relapses.

Curing MS may not be as simple as administering one antiviral or antibacterial medicine, but the study of infectious triggers offers insight into MS development, and new avenues for therapeutic strategies.

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