Small Study Shows Unexpected Reversal of Some MS Symptoms
I don’t usually write about drug studies, especially ones that are tiny and preliminary. But an unexpected result has peaked my interest in this one.
Researchers at The University of Queensland in Brisbane, Australia report that half of the progressive MS patients in their study of a treatment called ATA188 had a reversal of some of their symptoms. Now, there were only six patients studied and that’s a tiny, tiny number. And, this Phase I study was designed only to evaluate the safety of the treatment and identify possible side effects. The study wasn’t intended to measure the effectiveness of the treatment. But the researchers report symptoms improved for three of the six participants, starting two to eight weeks after the first infusion.
“One person with secondary progressive MS showed striking improvement,” said the report’s author, Michael Pender, MD, PhD, in a press release. “This participant had a significant increase in ambulation from 100 yards with a walker at the start of the study, and over the previous five years, to three quarters of a mile, and was now also able to walk shorter distances with only one-sided assistance. Lower leg spasms that had persisted for 20 years resolved,” he said. Pender said another participant, this one with primary progressive MS, showed improved color vision and visual acuity. All three participants had improvements in fatigue and ability to perform daily activities.
Treatment removes ‘rogue’ immune cells
The treatment being studied seems, in some ways, similar to the way Lemtrada and Ocrevus attempt to treat MS — by attacking specific cells in the body’s immune system. (Lemtrada attacks certain B and T cells, Orevus only certain B cells). It’s believed that “rogue” B and T cells may play a part in attacking the myelin sheath that protects nerves in the brain and spinal cord.
In this study researchers removed the participants’ own T-cells and then stimulated them to boost their ability to recognize and destroy cells infected with the Epstein-Barr virus. Some doctors believe there may be a connection between Epstein-Barr and multiple sclerosis. The researchers then injected participants with infusions of their modified T-cells every two weeks for six weeks. The patients were then followed for the next 26 weeks. The researchers hope that by eliminating the EBV-infected B-cells they may be able to reduce the destruction of myelin that occurs in MS.
Evidence mounts of MS-EBV connection
“The best responses were seen in the two people who received T-cells with the highest amount of reactivity to the Epstein-Barr virus,” Pender said. “Of course, much more research needs to be done with larger numbers of participants to confirm and further evaluate these findings, but the results add to the mounting evidence for a role of the Epstein-Barr virus infection in MS and set the stage for further clinical trials.”
These results were presented at the American Academy of Neurology’s 69th Annual Meeting in Boston, April 22-28, 2017.
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Keith Weiskamp
I'm glad that you took the time to report on this important science and research that is taking place. I would, however, like to pint out that your article is misleading and that I do believe you are missing some very important points. First, the very important premise that can't be overemphasized is that the researchers believe that a key cause of MS is the EPV virus. In particular, the research is pointing to the likelihood that the virus is able to attach itself to some B cells in the body and circulate. In a sense you could say that the virus is hijacking B cells. This research is wildly different than the research that went into drugs such as Lemtrada and Ocrevus.
In your article you state: "The treatment being studied seems, in some ways, similar to the way Lemtrada and Ocrevus attempt to treat MS — by attacking certain B-cells and/or T-cells in the body’s immune system." This is not all the case. The treatment does not really involve indiscriminately killing off B cells, which are very important to the immune system. Whjat the treatment involves is taking a patient's T cells, retraining them to recognize rogue or infected B cells, putting the T cells back, and then letting the T cells do their work to deplete the infected B cells. The drugs you mentioned are based on much older technologies and research and are are synthetic drugs that are mainly designed to wipe out a person's full population of circulating B cells. The problem with this approach is that it does not discriminate against "healthy" or infected" B cells and it leaves a patient at significant risk of not having their immune system protected. In other words, this new approach is very targeted whereas existing therapies are not very targeted.
The current research that is being done in this area is very important because (a) it is based on a model whereby the researchers believe they have isolated a key cause of MS and (b) the therapy being used (at least currently) comes from within the patient. Basically, the patient's own immune system is being retrained to do the job it needs to do. This is very different than simply disabling a key aspect of the immune system.
Ed Tobias
Hello Keith,
Thanks for taking the time to provide such detailed comments. But, I'm disappointed that you believe what I've written is misleading. It certainly wasn't intended to be.
My column was written from the viewpoint of an MS patient. As such, the finding that jumped out at me was that 50% of the patients in this tiny, preliminary study showed improvement in at least one symptom. As you know, very few MS DMDs affect symptoms in addition to halting progression. Yes, it's important to note that the EPV virus may prove to be linked to MS. But, from my point of view as a patient the headline is the possibility of having another DMD available that might offer symptom relief.
Reviewing what I wrote when I compared the ATA188 process to that of Lemtrada and Ocrevus, however, I see that I could have written a better explanation. When I wrote “...by attacking certain B-cells and/or T-cells in the body’s immune system" I was referring the fact that all three procedures attack immune system cells. I should have made it clear that Lemtrada attacks specific B cells and T cells while Ocrevus attacks specific B cells and is designed to continue to suppress those B cells. I intend to edit my column so that this is expressed more clearly.
I do think that I was very clear when I wrote: "In this study researchers removed the participants’ own T-cells and then stimulated them to boost their ability to recognize and destroy cells infected with the Epstein-Barr virus. Some doctors believe there may be a connection between Epstein-Barr and multiple sclerosis. The researchers then injected participants with infusions of their modified T-cells...."
And, I believe that you are incorrect when you write that Lemtrada and Ocrevus "wipe out a person’s full population of circulating B cells. The problem with this approach is that it does not discriminate against “healthy” or infected” B cells and it leaves a patient at significant risk of not having their immune system protected." As I understand it, Lemtrada selectively targets B and T cells that carry the CD52 protein. Ocrevus targets B-cells with the CD20 marker. I don't believe that either of those drugs will "wipe out a person's full population of circulating B cells."
I think that the idea of a treatment that retrains the patient's own immune system to do the job it needs to do is exciting. And, in fact, that's the hope of Lemtrada, i.e. that, though there's no outside cell stimulation as with ATA188, it's hoped that the B and T cells will return without the suspect CD52 protein.
Ed
Paul Hanten
This is the type of work that needs to be fast tracked. I have seen reports/studies like this and then they recycle every 10 years. This is a treatment I would do a Phase 3 study on for sure.
John Cordingley
As a secondary progressive-wheelchair-bound MS-patient no one needs to explain the urge for urgency. However, bypassing phase 1 and phase 2 trials would not be helpful or even sensible. The early phase trials are designed to ensure safety and establish dosing for the new, “hopeful”, drug. Personally, I long for new , safe treatment options but jumping straight to phase three trials with a promising new drug candidate would be putting the proverbial cart before the horse. Patience is very hard. I know, believe me but the trials have real method behind their madness. Allow others doing the research to do it thoroughly and carefully. We have had enough “thalidomide” experiences, let us learn from them! Very very sincerely, John Cordingley
Ed Tobias
The case you make is a good one, John. I agree.
Thanks for taking the time to comment.
Ed
Hugo
This is so good :) Phase I, yeah, but I am so happy to read this. More to come I can only hope.
Ed Tobias
Yes, let's hope that this leads to further study and positive results.
Ed
Pamela
This is the most encouraging article I have seen recently. I have PPMS and have always suspected it's link to Epstein Barr Virus. When I was 16 years old I was hospitalized for a week with EVB. It took months before I fully recovered. Or did I? Maybe it laid dormant in my system. I will be very interested in following this line of research.
Ed Tobias
Hi Pamela,
It's still very, very early but fingers are crossed that benefits will continue as larger, more controlled studies are done.
Ed
natania nunubiznez
This is similar to what happened to me! I was hospitalized at 17, and had severe nerve and aches and the doctors were confounded. EBV is what it was, and my MS is progressing, my EBV levels are high. Those are just facts. I would, however, like to be part of that clinical trial and would go to Australia to doit.
Ed Tobias
Hi Natania,
You might be interested in reading my MS Wire column that will be published Tuesday, April 24. It contains information about some new research involving EBV and MS.
Ed
Ton
Is there any way to access and participate in this trial in Argentina?
Ed Tobias
I don't know. I would suggest that you ask the primary researcher of the study, whose name and affiliation are included in my column.
Ed
Karla Starkey
I have had Ms S for 38 years. I had the Epstein Barr virus when I was 16. I am now 67 and have secondary progressive MS. I live in Houston, Texas. I now take ocrevus. I use a 3-wheel walker. If you know anything I can do please e-mail me. My doctor in Houston is very much into research. I always say I want to be normal before I die.
I do not have much time. I have had MS since I was 29.
Carrie Batton
I am beginning to agree with the EBV connection with MS. I was diagnosed with PPMS at age 48. My mother has had Rheumatoid Arthritis since her 40's which is another autoimmune disease. One of my brothers was diagnosed with Type 1 Diabetes in his early 30's known as LADA - Latent Autoimmune diabetes in adults. My other brother got Bell's Palsy which they say is caused by a viral infection of a latent virus that may provoke an autoimmune reaction against peripheral nerve myelin. My oldest daughter has Psoriasis which is also an autoimmune disease. The one connection in my family that makes sense to me would be the Epstein Barr virus. I hope they continue to research.