Is a Herpesvirus Messing with MS?

Multiple sclerosis (MS) is a puzzling and complex autoimmune disease. During MS the immune system attacks cells in the brain causing damage to and loss of the myelin protein that is produced by cells called oligodendrocytes. Myelin acts as an insulating sheath around nerve cells (like the rubber coating on electrical wires), and damage to myelin impairs normal nerve signal transmission. Depending on where the damage occurs in the brain, MS leads to various symptoms including muscle weakness, spasticity, vision problems, and a range of other effects. Since the damage (sclerosis) in the brain can occur at numerous sites (hence the name multiple sclerosis), the constellation of symptoms and severity can vary greatly in different individuals.

While the autoimmune nature of MS is clear, the causative factors that initiate the disease are far from evident and may not be the same for different patients. There is definitely a genetic component with certain genetic markers being associated with risk for disease development. There also appears to be various environmental risk factors that may trigger the onset of the disease, including smoking, vitamin D deficiency, childhood obesity, and viral infection. While each of these factors shows some association with MS, their precise roles remain poorly defined.

Among viruses, members of the herpesvirus family have been the most prominent candidates. The herpesvirus that causes mononucleosis, the Epstein-Barr virus (EBV), has been identified as a risk factor and remains an attractive agent for further study. In addition to EBV, a second herpesvirus known as human herpesvirus 6 (HHV6) has been implicated over the years, but the data were conflicting. It was subsequently determined that there are 2 closely related, but distinct types of HHV6 that are now designated HHV6A and HHV6B. A recent study in the journal Frontiers in Immunology indicates that the inability to distinguish between HHV6A and 6B was likely a confounding factor in early studies. This new study developed a test to differentiate 6A from 6B and looked for antibody levels against each virus in over 8000 MS patients versus matched controls. They found that MS patients had significantly higher anti-HHV6A levels than the controls while there was no difference in anti-HHV6B levels, implicating only HHV6A as having an association with MS. Importantly, they also examined old blood samples from MS patients prior to the onset of disease. Again compared to matched controls, the researchers found that individuals who went on to develop MS had higher anti-HHV6A levels even before the disease first appeared, with no difference in HHV6B levels. Finding higher HHV6A levels before disease onset is supportive of the hypothesis that this virus infection may contribute to disease development and not simply be something that occurred after MS began. Interestingly, it is known that HHV6A can infect oligodendrocytes while HHV6B cannot, and the researchers pose several testable ideas for how HHV6A infection of these cells could lead to loss of myelin. Someday a vaccine against HHV6A may help eliminate this virus as a potential trigger. For now it is way too early to know how these results might impact MS treatment or prevention, but it at least identifies another promising risk factor for future investigation.

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