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Rarely do articles published in scientific journals make the leap to the general press. Of the more than three million research manuscripts published each year, very few capture the interest of the non-specialized reader.
But recently it has happened once more. A study published in the journal
«Science» he has achieved it. It has been thanks to the high relationship that the authors have found between the risk of suffering from sclerosis multiple (MS) and the fact of being a carrier of a human herpesvirus called Epstein-Barr (VEB). Let us remember that this is responsible for mononucleosis (popularly known as the “kissing disease”, since it is transmitted by saliva).
What scientists have been able to observe is that, following EBV infection, increased the risk of MS by 32. This is a devastating disease that is due to the loss of a covering called myelin in the cells of the central nervous system (brain and spinal cord).
What does the recent study tell us?
The analyzes have been carried out between more than 10 million members of the US Army, from which several samples were taken over twenty years.
Of all of them, regarding half a million were negative for EBV when the study began, and of these, 35 developed multiple sclerosis following being infected during the study period.
Hundreds of other people, who were already positive for EBV when the project began, also developed the disease. Overall, of more than 800 individuals with multiple sclerosis, only one had not been infected with EBV.
In addition to studying this virus, the possibility that the “culprit” was another was studied. For this, antibodies once morest cytomegalovirus – which is also transmitted through saliva, such as EBV – and other herpesviruses were measured. But they found no difference between those who ended up with MS and those who didn’t.
Finally, by analyzing a protein whose levels increase when there is neuronal damage, they also ruled out that MS occurred before EBV infection.
With all this, they were able to conclude that the risk of suffering from the disease multiplied by 32 following Epstein-Barr infection, suggesting that the virus is the main cause of multiple sclerosis.
To confirm this, one more step is necessary.
Despite the strength of the data, we must be cautious. Because it is easy to fall into euphoria. But, strictly speaking, to affirm that this is the cause, it would be necessary to show that EBV prevention prevents MS. That is to say, if the virus was really responsible, preventing infection the disease should end. And this has not yet been proven.
In addition, we also need to understand the mechanism by which EBV causes the disease. It is probably mediated by something called mimetismo molecular and that usually appears in autoimmune diseases, due to the structural resemblance between some proteins of the virus and proteins of the nervous system.
On the other hand, it is important to note that, although everything indicates that the presence of the virus is necessary for the disease to appear, it is not a sufficient circumstance.
In fact, according to official figures, around 95% of the adult population has been infected with EBV at some point in your life. On many occasions, even without being aware of it.
After infection, the virus remains dormant forever in the B lymphocytes of those who suffer from it, becoming a carrier for life. But nevertheless, only one in 3,000 people lives with multiple sclerosis. So it is clear that other elements must be present for the disease to appear.
And now that?
For decades it has been argued that the cause of MS was unknown. However, if the hypothesis of this study is confirmed, how to deal with the disease would change radically. From now on we should begin to consider the MS as a complication of EBV infection.
This has some important considerations for both prevention and, above all, treatment of the disease. In this sense, it should be noted that for some years they have been using, with very good results, monoclonal antibodies to treat the sick.
These antibodies have the mission of attack B cells, which are the origin of the damage to the cells of the brain and spinal cord. Well, from now on it might make sense to refine the technique to specifically target EBV-infected B cells.
And the other strategy to consider goes through the development of a EBV vaccine, something that the pharmaceutical company is already working on Modern, the same one that has recently created a messenger RNA vaccine once morest covid-19.
Right now, the procedure with this vaccine is in the human trial and perhaps the current results will accelerate the development of this line of work to prevent infectious mononucleosis.
In any case, both options, for the time being, are no more than conjectures. Conjectures supported by some spectacular data, it is true, but only that, conjectures.
I hope everything is confirmed. Because, in that case, maybe it will open at the same time a new hope in the search for the origin of other neurodegenerative diseases whose cause remains unknown, as is the case with the diseasee Parkinson’s, Alzheimer’s or amyotrophic lateral sclerosis (ALS).
Jose Antonio Garrido Cardenas Professor of the Department of Biology and Geology, University of Almería.
Article originally published in
THE CONVERSATION
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