A recent report led by Alberto Ascherio, MD, PhD, a professor of epidemiology and nutrition at Harvard T.H. Chan School of Public Health, provides new, compelling evidence that EBV may be what triggers the immune process that leads to MS. RELATED: What Does the Epstein-Barr Virus Have to Do With Multiple Sclerosis?
EBV Appeared to Raise the Risk of MS While Other Viruses Didn’t
The study, published on January 13 in the journal Science, compiled data on more than 10 million U.S. military recruits — 955 of whom were diagnosed with MS during their time in service — over 20 years. Researchers discovered a 32-fold increase in MS risk after infection with EBV, but no increase in risk after other viral infections. A longitudinal analysis of this amount of data took investigators years, but it wasn’t a blind shot in the dark as to what they were looking for. Previous research has pointed to involvement of EBV, a virus known for, among other things, causing mononucleosis (mono or, in the juvenile vernacular “the kissing disease,” because it is most commonly spread via saliva). Most of the world’s population is infected with EBV in their youth and, even though the virus remains in the body’s systems for life, the vast majority do not go on to develop MS. This means there must also be other causative factors involved in the development of multiple sclerosis. Other possible risk factors for MS that have been identified in the past include smoking (and early exposure to secondhand smoke), vitamin D deficiency, and more. Approximately 900 gene variations are also suspected to be involved. But no other risk factor seems to stand out like infection with EBV. Within the group of military recruits studied, a small number had never been infected with EBV before. Of that subset of subjects who eventually were diagnosed with multiple sclerosis, 32 out of 33 contracted EBV before they developed MS.
Could MS Be Analogous to Long COVID?
Teasing out the causative factors in such an epidemiological study is tricky. Those of us with MS have highly (some might say overly) reactive immune systems. If those errant immune systems develop higher amounts of antibodies to viral infection, we may develop MS because of the body’s reaction to the virus and not the virus itself. Our societal understanding of these knock-on conditions has been heightened by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the disease it causes, COVID-19. Many will have heard the term “long COVID,” described in detail in October 2021 in JACC: Basic to Translational Science, which describes new or ongoing COVID-19 symptoms that linger for weeks or months after an initial infection. Long COVID has been associated with symptoms — such as fatigue, headache, shortness of breath, cough, chest pain, anxiety and depression, and deficits in smell and taste — and the onset of conditions such as fatty liver disease, kidney disease, fibromyalgia, chronic fatigue, and others continuing after or beginning as a result of COVID-19. I have to wonder about a similar correlation effect with EBV, mono, and multiple sclerosis. If the body’s reaction to SARS-CoV-2 post COVID-19 can be responsible for long COVID and its associated conditions, is it too big a step — as we digest the recently published findings — to think multiple sclerosis may be something of a “long mono” condition?
If So, Could an EBV Vaccine Prevent MS?
The hope, of course, is that the information gleaned in the new report will help advance both prevention and cure of MS. Of particular promise would be the concept of vaccinating against EBV infection as a way of preventing the onset of MS. Just as it appears we can avert long COVID by vaccination (which reduces both infection with or disease severity of COVID-19), might we be able to block this long mono effect by blocking EBV, thus averting MS? Will mRNA vaccine technology, employed with success in the COVID-19 fight, be a key to ending MS for the next generation? Might antiviral therapies (existing and under development) “cure,” or at least change the course of, the disease for those already living with multiple sclerosis? Is this new information the key, or simply another door to yet another corridor, in our search for an end to MS? Will I live long enough to find out the answers to these (and other) MS-related questions, or will those behind us be the only beneficiaries of this discovery? Dr. Ascherio and his colleagues have taken a step toward the possible beginning of what is sure to be a complicated answer to my questions — and that’s as strong a start as we’ve seen in my lifetime with MS. Wishing you and your family the best of health. Cheers, Trevis
