The virus is the door, but not everyone who walks through it gets sick
Durante décadas, la esclerosis múltiple ha sido una enfermedad cuyo origen permanecía en la penumbra; hoy, la ciencia señala con creciente firmeza al virus de Epstein-Barr como condición necesaria para su aparición. Un estudio monumental que siguió a diez millones de militares durante veinte años reveló que la infección multiplica por treinta y dos el riesgo de desarrollar la enfermedad, abriendo una pregunta que resuena en toda la neurología moderna: si podemos evitar el virus, ¿podemos evitar la enfermedad? La respuesta, como ocurre con las grandes preguntas médicas, es al mismo tiempo prometedora y profundamente incierta.
- Un hallazgo publicado en Science sacudió el campo de la neurología al establecer el virus de Epstein-Barr como precondición absoluta para el desarrollo de la esclerosis múltiple, reorientando décadas de investigación.
- La paradoja es inquietante: el 95% de la humanidad porta el virus, pero solo una fracción ínfima desarrolla la enfermedad, lo que sugiere que el virus es necesario pero no suficiente, y que otros factores genéticos o ambientales aún desconocidos determinan el desenlace.
- Investigadores como Xavier Montalban impulsan iniciativas globales para reunir a los principales expertos mundiales en el virus y diseñar vacunas preventivas que interrumpan la cadena antes de que la enfermedad se instale.
- La mayor amenaza para esta estrategia es biológica: algunas partículas del virus se asemejan a la mielina, la vaina protectora de los nervios, lo que significa que una vacuna mal diseñada podría desencadenar la misma respuesta autoinmune que pretende evitar.
- Neurólogas como Àngela Vidal y Yolanda Blanco advierten que, pese a la solidez del vínculo, la prevención fiable de la esclerosis múltiple sigue estando lejos del alcance clínico actual.
Un estudio publicado en Science en 2022, que siguió a más de diez millones de militares jóvenes durante dos décadas, llegó a una conclusión que ha reconfigurado la neurología: infectarse con el virus de Epstein-Barr —el responsable de la mononucleosis— multiplica por treinta y dos el riesgo de desarrollar esclerosis múltiple. Si el virus es una condición necesaria para que la enfermedad aparezca, la lógica es tentadora: prevenir la infección podría equivaler a prevenir la enfermedad.
Xavier Montalban, neurólogo y presidente del Centro de Esclerosis Múltiple de Cataluña, ve en este hallazgo una oportunidad concreta. Desde su iniciativa Mystery Souls, centrada íntegramente en el virus de Epstein-Barr, trabaja para reunir a los principales expertos mundiales y diseñar estrategias de vacunación preventiva. Sin embargo, reconoce que el camino es arduo: aún no se sabe con certeza si todos los casos de esclerosis múltiple están vinculados al virus, y el virus por sí solo no basta para causar la enfermedad.
Esa paradoja es el nudo central del problema. El 95% de la población mundial contrae el virus en algún momento de su vida, pero la inmensa mayoría nunca desarrolla esclerosis múltiple. Àngela Vidal, neuróloga del Hospital de Sant Pau, es directa al respecto: la estrategia preventiva es compleja y estamos lejos de poder evitar de forma fiable la aparición de la enfermedad. Demasiadas piezas del rompecabezas siguen sin encajar.
Yolanda Blanco, jefa de neurología del Hospital Clínic, comparte esa cautela y añade una advertencia técnica de peso. Algunas partículas del virus presentan una inquietante semejanza con la mielina, la cubierta protectora de las fibras nerviosas. Esto significa que una vacuna diseñada para atacar el virus podría, inadvertidamente, desencadenar la misma respuesta autoinmune que se pretende evitar. El horizonte preventivo existe, pero exige identificar con precisión qué elementos del virus atacar y cuáles dejar intactos.
A landmark study published in Science in early 2022 followed more than ten million young military personnel over two decades and arrived at a striking conclusion: infection with Epstein-Barr virus—the pathogen behind mononucleosis and the so-called kissing disease—increases the risk of developing multiple sclerosis by as much as thirty-two times. The finding has reframed how neurologists think about one of the nervous system's most debilitating autoimmune diseases. If the virus is truly a necessary precondition for the disease to emerge, the logic follows: prevent the virus, and you might prevent the disease itself.
Xavier Montalban, a neurologist and president of the Multiple Sclerosis Centre of Catalonia, frames the opportunity plainly. Once we understand that Epstein-Barr virus is an absolute requirement for multiple sclerosis to develop, he explains, we can begin designing vaccines to target the virus and block the disease before it starts. The challenge, he acknowledges, is formidable. Montalban leads a research initiative called Mystery Souls, which focuses entirely on the Epstein-Barr virus, and he notes that the field is preparing to convene the world's leading experts on the pathogen to discuss prevention strategies and how to mount an effective defense against it.
Yet the picture grows more complicated when you examine the numbers more closely. Ninety-five percent of the global population contracts Epstein-Barr virus at some point in their lives. The vast majority of these people never develop multiple sclerosis. This paradox sits at the heart of the scientific puzzle. Montalban himself acknowledges the uncertainty: researchers still do not know whether every case of multiple sclerosis is actually linked to Epstein-Barr infection. What they do know is that without the virus, the disease does not appear. But the virus alone is not sufficient to cause it.
Àngela Vidal, a neurologist at Hospital de Sant Pau, expresses skepticism about how soon prevention might become reality. The strategy is complicated, she says, and we remain far from a point where we can reliably prevent multiple sclerosis from appearing. The fundamental problem is that the virus affects nearly everyone but harms only a fraction of those infected. Too many pieces of the puzzle remain unclear. We know the infection is necessary, Vidal explains, but predicting whether we can prevent infection itself, or whether preventing infection would prevent the disease, remains beyond our current reach.
Yolanda Blanco, head of neurology at the Clínic hospital, shares this cautious view. The link between Epstein-Barr virus and multiple sclerosis is clear and strong, she confirms, and carrying the virus or testing positive for it substantially raises disease risk. But having the virus is necessary without being sufficient—a crucial distinction. Blanco sees promise in a preventive approach, though she emphasizes that success would require identifying precisely which viral particles or antigens could be targeted to stop multiple sclerosis from developing. Some of these particles, she notes, bear a troubling resemblance to myelin, the protective coating around nerve fibers. This similarity raises the possibility that a vaccine designed to attack the virus might inadvertently trigger the very autoimmune response it aims to prevent. The path forward exists, but it demands far greater understanding of which elements of the virus to target and which to avoid.
Notable Quotes
If you don't have an Epstein-Barr infection, you don't develop multiple sclerosis. But ninety-five percent of the population gets this virus and not all of them develop MS afterward.— Xavier Montalban, neurologist and president of the Multiple Sclerosis Centre of Catalonia
We remain far from achieving a point where multiple sclerosis doesn't appear. The strategy is complicated.— Àngela Vidal, neurologist at Hospital de Sant Pau
The Hearth Conversation Another angle on the story
So if ninety-five percent of people get this virus and most don't get MS, what exactly makes the difference between someone who gets sick and someone who doesn't?
That's the question keeping neurologists awake. We know the virus is absolutely necessary—you cannot develop MS without it. But something else has to be present too. Genetics, probably. Maybe environmental triggers. The virus is the door, but not everyone who walks through it gets the disease.
And if we could vaccinate people against Epstein-Barr before they ever got infected, would that solve the problem?
In theory, yes. But here's the trap: the virus is so common that most people are already infected by adulthood. And we still don't fully understand which parts of the virus actually trigger MS in susceptible people. If you vaccinate against the wrong particles, you might do nothing. Or worse, you might accidentally teach the immune system to attack the body's own nerve tissue.
So the researchers know what the problem is but not how to fix it yet.
Exactly. They've identified the necessary condition. Now they have to figure out the sufficient one. That's the work ahead.