In recent decades, mounting evidence has suggested the Epstein-Barr virus (EBV), a ubiquitous member of the herpes family that causes infectious mononucleosis (a.k.a. the “kissing disease”), can cause multiple sclerosis (MS). Last month, a study published in the journal Science went even further, citing EBV infection as likely the leading cause of MS. It is a compelling connection that begs many questions. For example, if someone has had mono – and 90 percent of U.S. adults have been exposed during their lifetime – should they worry about developing MS? Can they do anything to stop it? If we find a vaccine for EBV, can we prevent MS and possibly cure it? And what does this example of a viral link to an autoimmune disease tell us about potential future risks from COVID-19 infection? All are important questions for medical researchers, clinicians and, ultimately, patients and our society.
The suspected link between nervous system diseases and viruses is not new. In fact, many autoimmune diseases are thought to originate from something called “antigen mimicry.” Think of it as if the disease-causing agents, or “bad guys,” are wearing a kind of antigen “jacket.” Immune cells, the “good guys,” look for bad guys wearing this jacket to detect and destroy. In some instances, the good guys mistake one jacket for another and attack in a form of friendly fire. With MS, it’s thought the brain’s white matter mimics a bad-guy antigen.
Encephalitis lethargica or “sleepy disease,” first described in 1917, was followed by a Parkinson’s-like condition that was linked to the 1918 influenza pandemic. This story was told in the Oliver Sacks book Awakenings, which also inspired an iconic movie starring Robin Williams. Both tell the frightening story of how a simple viral infection “just the flu” years later triggered a crippling, relentless, and rare neurological disease.
As a neuroimmunologist specializing in MS and involved in post-COVID neurological complications research and treatment, I cannot help but wonder what we might see years after the current pandemic has ended. We are already seeing long-term immune reactions in people who have been infected. With one variant or another infecting most of humanity, will we see other unusual autoimmune diseases emerge decades from now? Another concern is that the COVID-19 virus might make old, “dormant” infections active again. EBV is one virus that has reportedly become re-activated during COVID-19 infection, as has herpes zoster. Could that potentially increase the risk of MS onset or new attacks?
Currently, there is no cure for MS, which often leads to disability and loss of employment. Until a cure is found, this latest study linking EVB to the disease makes it very plausible that a vaccine against EBV could dramatically reduce the burden of MS on patients and our society. However, we would need everyone to understand the benefit of this effort, and vaccine skepticism would pose a significant challenge.
Clearly, there are many important, unanswered questions and much work to be done. But we now have a clearer picture of where to focus our research efforts. This is positive news for those suffering from MS and, potentially, other autoimmune diseases.
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