Multiple sclerosis is a debilitating  disease that can cause all kinds of nasty symptoms, like vision loss,  fatigue, and loss of mobility.

And for many years, the cause of  this disease was totally unknown, and doctors could really only  tackle the symptoms as they came up, kind of whack-a-mole style. Thankfully, we now know what causes MS.

And knowing the cause of a thing is by far the best path to a cure, right? Except that the cause is a  virus that nearly everyone gets, and every attempt to develop a  vaccine for that virus has failed. All that said, will we ever find  a cure for MS?

Yes. But also, no. But also, probably?

Let me explain. [♪ INTRO] Multiple sclerosis affects around  3 million people worldwide. While MS often causes  disability, it’s rarely fatal. People often experience  muscle weakness and spasms, vision problems, dizziness, and other symptoms.

The disease will progress  differently in different people. For example, in relapsing-remitting MS, symptoms will occur in the form of “attacks,” between which everything is mostly ok. Meanwhile, in the various  progressive forms of the disease, symptoms will worsen steadily over time.

And while the underlying cause was a mystery for ages, we have known the basic mechanism of what’s causing  those symptoms for a while. MS causes the immune system to attack a specific part of the nerve cells called myelin. That myelin surrounds neurons  of the central nervous system, and both protects the nerves and  helps them transmit signals faster.

And when those neurons lose their  myelin and get sent out of whack, movement and coordination  gets a whole lot trickier. But why the immune system does  this has been a harder question. For a while, researchers had begun to suspect the root cause might be  Epstein-Barr virus, or EBV.

The virus that causes infectious  mononucleosis, aka mono, aka that really bad sore throat you got after making out with your lab partner in high school. And while mono can be a serious  infection right when you get it, researchers are only recently  learning how it relates to MS. New research has helped us be just about as sure as scientists can be that EBV is connected to MS, and we’ll get to why they’re so  confident about that in a second.

But there’s a puzzle that no  one has really solved yet, and it has to do with just how common EBV is. About 95% of people get  infected with EBV at some point in their lives, but only 0.04%  of the population develops MS. So there’s definitely something  else that we’re missing here.

Like, if 95% of people ate  cheeseburgers, and 0.04% of them developed a rare cheeseburger-induced disease, doctors would be looking for  more specific things those people had in common long before  they blamed the cheeseburgers. Maybe in the toppings bar, or something. Still, the suspicion around a  link between EBV and MS was strong enough that one group of researchers  decided to pull blood samples from ten million US servicemembers  to trace the connection.

And the sample needed to be that  big, because MS is so rare that under a thousand people in that  entire sample actually had it. But they got what they needed,  and the researchers were basically able to show things always  happening in the following order: First, an individual’s blood  would test positive for EBV. Then they would develop markers  that suggested nerve damage, without showing MS symptoms.

And then they’d start showing MS symptoms. And they were able to show that no other variable accounted for the emergence of MS. So once they knew for sure that  EBV was the underlying cause of MS, scientists rushed to work  out exactly how it does that.

And efforts are ongoing, but  it seems to be at least partly a result of the immune system trying to chase down EBV and getting confused along the way. A 2023 study in the journal  Science Advances showed that there’s actually a good  reason for this confusion. The researchers demonstrated  that in some MS patients, immune cells are capable of  targeting both an EBV protein called EBNA1, and a myelin protein called CRYAB.

Probably because EBNA1 and CRYAB have a short segment that’s literally identical. So those poor immune cells are just doing their job of keeping EBV under control. They can’t help that they just  happen to stick to an identical sequence that we happen to  be using, not just the virus.

When you put it all together,  it seems to go like this: EBV infects antibody producing  immune cells called B cells, and a different kind of immune cell  called T cells try to shut down that infection. But they end  up targeting myelin instead. Which means that treatments aimed  at either the infected B cells or the overactive T cells might  help to tamp down symptoms of MS.

A lot of current treatment strategies are aimed at slowing down these immune cells. There are fortunately a bunch of options, and we’ll include a good summary in  the video description, but in brief: Steroids can tamp down the severity of an ongoing attack by dampening the immune response. Antibody-based treatments target immune cells directly and slow down their response.

And other types of medications may reduce the frequency of MS attacks. It’s great for MS patients  that all those things exist, but if the cause is a virus, and  we vaccinate against that virus, MS goes away forever, right? Well, right, but the problem is that EBV is a stubborn piece of… Something I can’t say here.

It’s not like they haven’t tried  to vaccinate against the thing. But for a virus, EBV is ridiculously complex. It infects multiple types of  cells, has a life cycle that takes place in multiple phases, and it even has multiple layers to its structure… Just picking the right part of the virus to try to vaccinate against has been a struggle.

For example, a lot of efforts have targeted a molecule called gp350 on  the surface of the virus. None of them have been approved. One of the most successful candidates  was abandoned when it turned out to prevent the symptoms of mono,  but not infection with the virus.

Although some researchers have suggested that this one’s worth another look. After all, since MS is caused by  our immune system going too far, and the vaccine tamps down the  immune system’s response to EBV, that might be enough. Other vaccine candidates include  gp350 alongside other proteins.

And, an mRNA vaccine that incorporates a couple of different sequences is in trials at  the time we’re writing this video. Of course, even if we had a working vaccine in hand, for it to truly stop MS, we’d have to get that vaccine to… everybody. And a discussion of how hard that would be is a video on its own, but trust me.

It’s hard. But here’s the good news: a vaccine isn’t the only thing we can do here. One theoretical treatment approach could be to target those confused T  cells we talked about earlier.

Or you could target the B cells  where EBV likes to hide out. There’s one approved drug, called ocrelizumab, that already does that. And we can always just try throwing some good old antiviral drugs at the problem.

So what I’m trying to say  here is: There are options. It might be cheesy to say that knowledge is power, but in this case, it’s even more true than usual. To explain what I said in the  beginning: Will we ever cure MS?

Well, yes, because we know the cause. But no, because we may never eradicate EBV. But probably, because we have a lot of other options to pursue going forward.

This episode was brought to you by this month’s President of Science Mclaren Stanley. Thank you so much for being awesome. And if you want to learn more about becoming the next President of Science, head over to Patreon.com/SciShow, and thanks for watching. [♪ OUTRO]