Here's a link to the article [0].

Just a bit of background - 95% of humans will experience infection with EBV at some point in their lives. Once you're infected, it remains latent, only flaring up in particular circumstances. MS is an autoimmune disease, like many others, and this paper does not imply that EBV directly causes MS. Obviously, as so many more people have EBV than have MS, EBV infection does not completely explain why people get MS.

Just to put a small caveat to the paper. The comparison is to EBV 'seronegative' population - this is a minority of people (i.e. people who do not have evidence of being infected with EBV). You could argue this is an 'unusual' population in the first place and there's something about them that provides protection from MS.

Another point is that EBV is a risk factor, there are other risk factors known too. I think the key to understanding a lot of autoimmune diseases is to understand how our adaptive immune system works. Our immune response is a very complex cell-to-cell interaction between millions of cells all with different roles, and how the immune system decides whether something is a threat or not is not, and how to respond to it, is not yet clear.

[0] https://www.science.org/doi/10.1126/science.abj8222

I have MS and my first relapse was a pretty textbook case of transverse myelitis of the sort that the EBV can cause.

I know some people have been asking about why that might be the case when a ton of people have EBV, and I think the causality may go the other way: Those of us with something wrong are more likely to both have EBV complications and MS.

There are other viruses like this as well (ones that most people get/have but aren't dangerous). I was on one medication where I needed to be tested monthly because if I got one particular (normally harmless) virus, the suppression caused by the medication meant I would probably die.

There's pretty clearly some sort of relation between the state of one's immune system + how it deals with 'benign' viruses + auto-immunity, and I'm excited to see what the future holds, but for now it's a cool confirmation of something a lot of MSers have talked about amongst ourselves for a while.

What is interesting is that Epstein-Barr has been reported to be related to Multiple Sclerosis since the early 1980s.


It is great if there is new information and if this leads to knowledge on how to reduce the chance of getting MS.

Cause is still not well explained. EBV is such an ubiquitous virus, more than 90% of all adults worldwide have been infected with it. Most will never know. Why is that just a tiny percentage develop MS?
This study appears to suggest that MS is essentially "long Epstein-Barr." Terrifying if the same pattern holds for covid, given the number of people who have some sequelae (the most conservative estimates are 2-5% for "serious" post-viral symptoms, which would be hundreds of millions of people worldwide). There will be an extraordinary amount of suffering, not to mention radical shifts in economic and public policy.
Terrifying - I was EBV positive 4 years ago. It does not mention an association between EBV severity and MS, but I was very symptomatic and had post viral fatigue for around a year. I had no idea about the MS association!
From my understanding, the leading theory of what causes autoimmune diseases is viruses. The immune system responds to the virus and ends up mistakenly attacking the body as well. This seems to support that, and shows that different viruses cause different autoimmune diseases.

More info: https://www.nature.com/articles/d41586-021-01835-w

This is a bit off topic but I have a question about causality.

Is causality really a fuzzy concept? For example I assume if action A causes event B I assume the connection is 100%. Can we really say that action A has a 30% chance of causing event B?

I ask because the more I think about it, when someone says action A causes a 30% chance of event B occurring what he is technically saying is action A is one causative factor that must occur and that we're missing information about other causative factors.

In the case of this article. A causative link is established between EBV and MS to a fuzzy probable degree. This seems to me that technically what's actually occurring is that a fuzzy causal link simply means that there are other causative factors we don't yet know about, and likely this is a specific type of immune system that reacts to EBV in a certain way.

Would my assessment be accurate? All causal connections are either 100% and any fuzziness just means we're missing information about other joint causal events that must occur to trigger the outcome. Does anyone who's a statistician know?

Contrary to the HN title, the paper is not about causal inference, it is a case-control study. A good primer on the limitations of case-control studies can be found here: https://www.medicalnewstoday.com/articles/280936#limitations
The parallel to Guillan Barré Syndrome seems intuitive. MS and GBS are both autoimmune disorders which damage myelin. MS is slower and chronic while GBS is acute and rarely relapses. What if MS is a low grade persistent immune response to a chronic viral infection such that those bad antibodies are created in small amounts indefinitely?
I wonder if MS is like the EBV version of shingles: if you don't get it early, when you do, it's a much worse disease. Most people pick it up early, but those who manage to avoid it and then get it late are in danger. Another instance of hygiene hypothesis.
I was wondering what the genetic factors are that cause EBV to push people to get MS and found this excellent paper [1] (see the genetic susceptibility section).

[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334604/

[2] https://www.google.com/search?q=genetic+factors+that+cause+E...

Interestingly, Moderna has some trial for mRna vaccine for Epstein-Barr virus [0]

[0]- https://www.clinicaltrialsarena.com/news/moderna-ebv-vaccine...

It's weird to me that they say 35 of the 801 MS cases were negative then positive before getting MS. The control group had 107 of 1566 were negative, but they don't bother to tell us how many of them ended up positive.

I assume enlisting is a high-risk place to get EBV, and without info on the control I don't see how you can draw conclusions. But I'm basing this on the summary rather than the actual article: does the article have the info?

I wonder how many viruses infecting humans we know nothing about just because they don't cause any obvious symptoms.
there is an experimental[0] treatment for MS, the "immune system reboot". i am a layperson but my understanding is stem cells are taken from the patient, the immune system is "destroyed" through immunosuppressants and the stem cells are then used to rebuild a "naive" immune system in the patient.

based on the info in the OP, i wonder if the MS result from EBV is random; what is the probability of a rebooted immune system to follow the same path after exposure?

[0] - https://www.nih.gov/news-events/nih-research-matters/immune-...

This featured quite heavily in todays issue of The RECC’E I put out this morning! Worth a quick read if you like quick- fact insights https://email.recce.news/a7i9l9x8y1
An interesting talk about someone who was able to reverse a lot of her MS symptoms with a change in diet: https://www.youtube.com/watch?v=KLjgBLwH3Wc
Here's a John McDougall talk, he had some close ties to Dr Swank, known for a lot of early MS research.


tldw: When your stomach layer is compromised, unprocessed food gets into your body. Food like animal protein, similar to our proteins, get attacked by the immune system, some of your cells are also mistakenly attacked.

Anyone with the compromised stomach is at greater risk for auto immune diseases. For example look of rates of ms among celiac or crohn's sufferers.

Same goes for type 1 diabetics, also autoimmune. Research suggests casein from dairy gets in the body, your immune system accidentally attacks your pancreas insulin making cells.


Is anybody testing for virus/bacteria vs virus/bacteria interactions?
Glad that we might eventually get rid of diseases from starting, but when it comes to a cure, research is unbalanced towards treating instead, because it makes more money.
I will read this but as someone who has had a family member diagnosed with MS if there are other connections or papers people can recommend I would be very grateful.
> and the team identified 1566 matched controls for them.

Can anyone please shed some light on this? How would this work?

Moderna are trialing an EBV vaccine. If it's successful, I wonder if we will see an end to MS. A cure would be great but failing that a prevention is almost as good.
Dr. Terry Walhs was diagnosed with MS and became wheel chair bound. She came up with a protocol that was able to reverse her MS. I recall from previous interviews that her theory was that MS was a disease of the mitochondria. https://terrywahls.com/
For more on EBV, I've discussed it on my blog here: https://denovo.substack.com/p/epstein-barr-virus-more-maladi...

(It doesn't just cause MS!)

This might explain why between 1992 and 2017 interferons were the go-to treatment for MS. Interferons (IFNs) are a group of signaling proteins made and released by host cells in response to the presence of several viruses. A virus-infected cell will release interferons causing nearby cells to heighten their anti-viral defenses.

After my diagnosis I personally went on Avonex (an interferon) in 2000, which was the only disease-modifying treatment (DMT) for MS at the time. My neurologist told me that they had no idea why interferons worked for MS, but they proved to be relatively safe and effective as slowing both clinical and symptomatic progression of MS. Naturally I asked the question to all my doctors, "Can a virus in the CNS be involved in triggering T-cells to cross the blood-brain barrier?" They would usually respond, "That's as good an explanation as any."

So I religiously stayed on interferons through to 2014, when the FDA approved an oral medication for MS. By that time I was really getting tired of the constant injections (I hate needles), and my MS had caused minimal problems for me up to that time, so I decided to give the non-interferon DMT it a try. The clinal trial data for this non-interferon medication looked promising. But in the year I was on the non-interferon DMT my MS progressed, and I didn't go back to interferons until after things culminated in a serious attack (relapse). I currently live with a lot of symptoms from new lesions that formed in my spinal cord in that year I was off interferons.

This experience had an impact on how I approach problems in general. These days I'm a lot more likely to stick with technology that is tried and true for any particular problem, even if that older technology is a little painful to set up and use. If it's been working fine up until now, don't rock the boat just because another option has come along.

Of course this doesn't mean I'm inclined to always only ever use old technology. If something very clearly superior comes along that has overhelming evidence of effectiveness, I'm open to changing. In 2017 I made the switch to Ocrelizumab, which is a monoclonal antibody that knocks down your B cells. The data from that was so compelling that I realized that was the right thing to move to from interferons. In hindsight, that has been a much better move than my disastrous experiment with the oral meds.

This recent study relating to EBV confirms my personal suspicions about the role of a virus in the development and progression of MS. Hopefully what this means is that therapies will come along that specifically target proteins only in EBV so that I can get my B cells back, since one of the consequences that a medical study I was in last year revealed is that my body doesn't produce antibodies in response to the COVID vaccine. I'd really like to get antibodies again, since I imagine that could give me more protection than what I get from the other immune cells I have.

If MS is a faulty immune response from EBV, wouldn't a vaccine theoretically and potentially trigger this same faulty immune response?

There are obviously other causative factors influencing MS. One is EBV, the other is likely a specific type of immune system.

I wish I was still a virgin.
I saw this news item last night, posted next to that one...

"Study finds hydroxychloroquine delays disability for least treatable form of multiple sclerosis" [0]

[0]: https://medicalxpress.com/news/2022-01-hydroxychloroquine-di...