A New Therapy Attacking a Common Virus Shows Huge Promise For Multiple Sclerosis

A treatment designed to attack a common virus that hides in our bodies could ease the decline caused by multiple sclerosis (MS), according to new trial results. Excitingly, it may even reverse some of the symptoms.

A phase 1 clinical trial by the California-based immunotherapy company Atara Biotherapeutics confirms latent Epstein-Barr (EBV) infections are viable targets for treating MS in at least some patients, reinforcing a curious link between the virus and a deadly illness that affects millions around the world.

Out of the trial's 24 volunteers, 20 showed signs of either improvement or at least a halt in their health's steady decline. Importantly, there were no signs of serious side effects.

Promising as these results might seem, the study hasn't yet been peer reviewed. What's more, the path from small clinical trials to approved medicine is a rocky one. Years of research based on larger, ever more diverse groups of volunteers are needed to reveal hidden risks or demonstrate the worth of the treatment.

But there's good reason to think targeting the dormant virus could be key to putting the brakes on a particular aspect of MS – progressive decay of myelin, the 'insulation' protecting nerve cells.

Around 95 percent of people catch EBV at some point in their lives; the virus, also known as human herpesvirus 4, causes the illness known as mono, or glandular fever.

Symptoms are rarely severe, but the virus sticks around in the body, ready for potential future reactivation. The consequences of its reappearance range from benign to deadly, although most people don't notice if EBV pipes up again.

However, research has now uncovered suspected links between EBV and various autoimmune diseases, cancers, and chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

As far back as the early 1980s medical researchers were noticing that an inordinate number of blood samples from people with MS had elevated levels of Epstein-Barr virus antibodies.

How the two might be related is an ongoing question, though a recent longitudinal study published by researchers at Harvard found that an EBV infection "greatly increased the risk of subsequent multiple sclerosis".

Another recent study by Stanford University researchers showed nearly a quarter of MS patients have antibodies that bind to both an EBV protein called EBNA1 and a protein produced by our own nervous system called glial cell adhesion molecule, or GlialCAM.

"Part of the EBV protein mimics your own host protein – in this case, GlialCAM, found in the insulating sheath on nerves," says Stanford immunologist William Robinson.

"This means that when the immune system attacks EBV to clear the virus, it also ends up targeting GlialCAM in the myelin."

That loss of myelin could be what's primarily responsible for the diverse symptoms of multiple sclerosis. These range from difficulty walking to cognitive dysfunction, numbness and tingling, and in some cases, pain, problems with vision, and even clinical depression.

Why EBV tricks the immune systems of some people and not others isn't known, though genetics might play some kind of predisposing role, possibly making it harder for their own white blood cells to respond to recurring EBV infections.

If the constant presence of the virus triggers some people's immune systems to attack their own myelin, helping them clear the infection could help treat MS symptoms as a result. This idea was first tested just under a decade ago, through the transfer of EBV-targeting immune cells into a single 42-year-old patient.

Encouraged by the experiment's results, researchers in Australia ran a slightly larger study on 10 patients back in 2018, taking the patients' own T cells and training them to hunt down virus-laden cells. With seven of the 10 showing signs of improvement, an even larger, more rigorous clinical trial was called for to really put the concept to the test.

Instead of using the patients' own cells, this latest trial by Atara Biotherapeutics relied on specially-selected donor white blood cells, hoping it might provide a more rapid, 'off-the-shelf' delivery system.

Called ATA188, they hope the therapy may not only give MS patients a chance to stay on top of EBV infection and thus improve their symptoms, but the 'donor model' would be easily scaled up to reach a greater number and higher diversity of patients.

The team's findings were presented at an investor meeting recently and a conference late last year. They claimed that of the 18 patients who agreed to participate in a more extensive data-collection period, nine reported a sustained improvement in their disability over a year or more.

There were also no reports of adverse immune responses, further demonstrating a strong need to continue research. Most exciting of all, the study also evaluated the regrowth of myelin.

Keeping in mind the small sample size and moderate improvements, the fact there are hints of re-myelination around some nerves provides solid ground for hope, since this is not something typically seen in MS patients.

"When a patient reaches a certain level of advanced disability, it is rare for them to naturally revert, and any improvement that is sustained would not be expected from the natural history of the disease," says University of Ottawa neurologist Mark Freedman.

With nearly 1 million people living with MS in the US alone, an illness that not only compromises quality of life but can shorten lifespans by years, a treatment that puts on the brakes can't come soon enough.

I guess if I had MS, I might try ti, as MS is a horrible way to die. Thus the jab couldn't be much worse, and perhaps might make me die quicker than the slow death by MS.

Shame that all these supposedly new drugs I hear about makes me skeptical that any of them are worth anything remotely close to the claims.

I certainly do not blame you. My step-grandmother had it, and it’s a horrible way to go. Let us know if you get to try it, and report how it went. I pray it does work, to A) help you and others suffering from MS, and B) to restore some of my faith back into the medical profession and pharmaceutical developers. Right now my faith in both have suffered greatly, and deservedly so in my opinion.

Just out of curiosity, have you ahd testosterone levels checked, if you are male?

There was a study a long time ago which tested symptomatic duration of EBV infection among normal people, vs self-reported steroid-abusing body-builders. It found the average course of illness of EBV among normal people was 2-3 weeks, but it was shortened to 2-3 days in the steroid users, who were confirmed with a blood test to have elevated androgens. The theory was EBV somehow used a receptor to get in cells which the testosterone was binding and thus preventing cell entry, or test somehow altered immune function enough to quickly wipe out the virus. The study hit me, because when I was a teen, EBV went around and knocked a lot of kids out of school, but a friend who used steroids got really horribly sick for about half a day, I thought it got him and he was going to be gone for a few weeks, and he was back to normal the next day.

Test “replacement” in older people is fairly normal, and might offer some benefit. I would try a month or two pumping it up to the top of the reference range, and see if there is any difference.

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