#BlackSwan: anecdotal evidence we can’t ignore

Barts-MS rose-tinted-odometer: ★★★★★

What is a black swan event? 

“The black swan theory or theory of black swan events is a metaphor that describes an event that comes as a surprise, has a major effect, and is often inappropriately rationalised after the fact with the benefit of hindsight”. (Source Wikipedia)

The case study below is another example of a mounting number of case studies of patients with MS being treated with antivirals, with activity against EBV, doing well. We now need to do properly powered randomised controlled trials to test the EBV causation of MS hypothesis definitively. 

Prof. Julian Gold and I launched the Charcot Project in 2012 to investigate the viral aeitology of MS. We tried on numerous occasions to get trials funded to test this hypothesis and have failed. We managed to test one anti-retroviral in a small proof-of-concept study, which was negative. Since then we have managed to get funding to see if famciclovir is capable of suppressing EBV shedding in the saliva. This study should have been completed by now, but we had to delay its start because of the COVID-19 pandemic. 

We have also managed to show that teriflunomide is anti-EBV in that it reduces EBV viral shedding in the saliva of people with MS. I suspect this is a very relevant an important observation and underpins the iTeri study, i.e. to use a B-cell depleting agent as induction therapy and teriflunomide or related compound as a maintenance therapy to prevent EBV reinfecting B-cells during the B-cell reconstitution phase. 

Life is short and I started working on EBV as a cause of MS way back in 2005 and feel like I am treading water. The evidence that EBV is the cause of MS is so overwhelming that we really can’t afford to ignore it any longer. What we need is a substantial investment from the major funding agencies, MS charities, wealthy philanthropists and Pharmaceutical companies with antiviral drugs in their portfolio to prove (or disprove) that EBV is the cause of MS. 

When you apply Bradford-Hill’s causation theory to EBV being the cause of MS  there is only one criterion out of nine that still needs to be ticked and that is experimental evidence. What we need are therapeutic interventional trials targeting EBV to complete the proof. 

Torkildsen et al. Tenofovir as a treatment option for multiple sclerosis. Mult Scler Relat Disord 2020 Oct 7;46:102569. doi: 10.1016/j.msard.2020.102569.

Some antiretroviral medications are also inhibitors of EBV. We describe a patient with highly active MS who was infected with HIV and started HIV-treatment containing tenofovir alafenamide (TAF), a potent inhibitor of EBV lytic reactivation. Her MS was in complete remission during this treatment, and she had new radiological disease activity again after switching to tenofovir disoproxil fumarate, an HIV drug with less potent activity against EBV replication. Based on the recently detected mechanism of TDF and TAF, we suggest that further studies on these drugs in MS are warranted.

CoI: multiple

Twitter: @gavinGiovannoni  Medium: @gavin_24211

89 thoughts on “#BlackSwan: anecdotal evidence we can’t ignore”

  1. What is the latest with that small Geneva-based biotech working on this front as well? Are they doing much?

  2. Could you envisage antiviral being prescribed to somebody with secondary progressive MS who is not on medication but has previously been treated with alemtuzumab?

  3. Could you envisage antivirals helping progressive MS if the person is not on any medication but has had alemtuzumab in the past?

    1. Ocrelizumab that is licensed for PPMS is an anti-EBV drug. So yes, I think these therapies will help people with progressive MS.

      The Atara trials of anti-EBV cytotoxic T-lymphocytes are targeting progressive MS.

      1. Can you please share evidence that OCR is anti-EBV? Assuming you are not referring to anti-CD20 B-cell the mode of mechanism for anti-EBV.

  4. The example you give is based on HIV patient and the effects of ebv antiviral will be amplified because the immune is under attack by the hiv virus. But let says you are right. But we both know this will go no where as pharma (turkeys) will not vote for Christmas. So how do you break this stalemate. Oh here’s idea crowd fund the trial if people are willing to pay £50000 for HSTC. Charge those who want to participate in the trial, and allow once money raised to finish the trial, participate on compassionate basis.

  5. Prof G,

    “Life is short and I started working on EBV as a cause of MS way back in 2005 and feel like I am treading water.”

    And it’s shorter for those of us with MS + it’s a progressively disabling life after DX with MS.

    These posts themselves are like Black Swans – they come out of the blue, create a bit of hot air, and then disappear again until the next time. Nothing changes! I was an attendee at the Research Day events and got over excited by the prospect of an anti viral – but we still haven’t got off first base. I don’t blame you, but the systems the science community has created to “protect us”.

    The anti viral approach (assuming it’s successful) would destroy the ever growing MS research community and take a huge chunk of the value of most pharma companies who sell MS therapies. They (both) won’t allow that to happen.

    Unless action is taken (which includes a willingness to push the current constraints to the limits), there is no point posting about Black Swans. When you retire you can enjoy your fine wine (I’ll be six foot under by then). But I suspect you’ll live with the regret that decades were wasted dampening down or destroying MSers’ immune systems, for little long term benefit, whereas some antivirals could have changed the lives of tens of thousands of MSers.

    I can see a nice trial of tenofovir + metformin. Both are safe. One would address the cause of smouldering MS and the other would promote some repair. The safety profiles of both drugs are well known. Oh, Silly me, it will take ten years to get through Phase 3, no one will fund it….

    1. “So we beat on, boats against the current, borne back ceaselessly into the past.” ― F. Scott Fitzgerald, The Great Gatsby

      I am still relatively young; maybe another 20 years left in me as an active MS researcher. I have time and energy so who knows where this will end up?

      1. MS deprived me of a retirement. Staying on beyond your sell by date will be a mistake. I’d suggest 60, 65 tops. If you push beyond this, the trainee neuros will be thinking “there’s that old fart Giovannoni, spouting the same old dogma”. We need some young Turks who will bring new ideas and challenge the system.

        “What do you call a person who is happy on a Monday? Retired.”

      2. Once again, you’re shooting at the wrong target. Time to get those sights recalibrated.

      3. Heres a thought experiment. I travel in time to 20 years forward and time years back and the same debate is still raging. The person who initiates the debate has been unable to move the findings to clinical practice. So who is the target? Let’s say pharma. But then of your team say you can’t get anything done without. Let’s MS patients for not putting up the funds. As John major once said put up or shut up. But Ms patients aren’t being asked to fund a cure to my knowledge. Could it be barts use these articles to bait pharma for funding? So now tell me who should be the target? I blame Donald Trump

      4. You can’t beat someone who won’t give up eh PGG (great Gatsby Goivanni lol)

        “decades were wasted dampening down or destroying MSers’ immune systems, for little long term benefit, whereas some antivirals could have changed the lives of tens of thousands of MSers”

        Sid you talk a lot of sense amigo

      5. Feathers,

        Read this short article:


        Praise has to be earned. A lot of people are making careers and money out of this vile disease. I’m not content with the “science is slow” excuse. MS is a devastating disease and yet we are still at the testing hypotheses stage. My GP has two patients in their mid 30s who have MS and are in care homes. It’s not an academic issue to these patients- it’s a loss of career, dreams, dignity. The slowness of real breakthroughs and treatments which stop this disease suggests that those in pharma and research don’t really appreciate how gruesome it is.

      6. Again, you talk a lot of sense Sid (and everyone else)

        I will be very upset to reach retirement age if I am honest ..

        It would take too long to list all of the losses I am constantly having to adapt too – it’s the difference between being alive and actually living – I’m 46 and have been robbed of hope for the last 25 years,but I’m glad I didn’t spend the last 25 years ruminating too much about it

        But man it sticks in my throat that no cure has been funded or found, despite the BILLIONS we generate; we go round in ridiculous circles and are expected to accept our decline
        and loss of pretty much everything regardless

        Not sure what the relevance of the MS champions link was?
        To be honest being independent is the last dignity I am clinging onto …so I think I’ll pass and hope they redirect their funds to finding a cure? Or is that what you mean…that we provide jobs for people…

        Finally, if an anti viral EBV meds have any hope of working or helping, then just be done with it and let us try ffs

        Your happy for us to take amantidine for fatigue and that was originally an influenza antiviral…

        Sid is right; it is gruesome being progressive-inconceivable and incomprehensible until you get there
        – desperate,I’ve started taking citicholine following on from our esteemed MDs post six years ago


      7. Maybe Aslan003 could be an ace up your sleeve.
        Seems 30 times more potent DHODH inhibitor than Teri as well as very good antiviral.

        Are there any phase 3 trials planned for MS Prof G? You’re lead investigator for this molecule, aren’t you?

      1. Recently published – tenofovir prodrugs (TDF and TAF) are extremely safe drugs and also potent inhibitors of EBV – TAF is better than the gold standard (ganciclovir) for EBV and 35x better than acyclovir


        TAF has virtually no side effects and is considered extremely safe – great for testing the EBV hypothesis in a trial for MS

  6. When people are diagnosed with ms, are tests run for EBV? If so, is anybody collating the data? Seems a good place to start?

    1. 100% of people with MS have EBV. Those who test negative are almost always positive when using more sensitive state-of-the-art assays. The studies showing that a small proportion of EBV negative pwMS did not use the definitive gold-standard immunofluorescence assay.

      1. Thank you! I hadn’t realised..
        Regarding Ocrelizumab, do you think this would help then if “no current inflammation “

      2. But in those 5% of people who are EBV negative the risk of getting MS is close to zero.

      3. It depends on how often you test. Over a three month period with weekly saliva samples ~45% shed. This compared to about 20% for normal healthy volunteers.

      4. This is a fairly alarming stat and makes you wonder why more resources have not been thrown at it previously. I understand the Pharma cash cow angle but what of the NHS (amongst other health authorities, insurance cos etc.) that spends millions on these drugs each year. Anyway, back to the Science – if Ocrelizumab is an anti-EBV drug, is it just that Teri is a more potent anti-viral and therefore has the potential for greater effect? Also, does it penetrate the BBB? sorry….I am no scientist but i am just trying to follow the logic through. If the B-cells are depleted and then teri is used to prevent reinfection this would avoid the need for Ocrelizumab over the longer term i.e. safety benefit. However, what of the disease that has established within the CNS and the smoldering element?

      5. I think we need to rationalise why various ‘anti-viral’ drugs are being considered:
        Amantadine: M2 proton channel blocker
        Does EBV express any of these channels?
        Ocrelizumab: An anti-CD20 antibody. This targets B-cells which express CD20, so presumably it depletes the EBV reservoirs rather than being directly ‘anti-viral’.
        Leflunomide and Teriflunomide: Inhibitors of protein kinase activity and pyrimidine synthesis which inhibits the herpes family of viruses.
        Valaciclovir/Famciclovir/Aciclovir: Thymidine kinase blockers which inhibit viral replication, but don’t work brilliantly when the virus uses intracellular elements to replicate.

    1. For people to adopt an innovation or a new treatment you need class 1 evidence and that takes well-designed large studies. This is why producing facts, which are based on quality data, takes time and money.

      1. EBM, “the conscientious, explicit and judicious use of current best evidence in making decisions about the care of individual patients“. At no point does this definition state that you can’t rely on grade 5 evidence, if it is the current best evidence. This doesn’t say you must wait 30 years or more for somebody to conclude a meta-analysis of double blind, randomised controlled trials before making any decisions. As an expert in the field your opinion constitutes this grade 5 evidence. NICE has subverted EBM and it’s decisions are not synonymous. NICE is a political tool to ration health services to a £20k Incremental Cost Effectiveness Ratio and stifle health innovation.

      2. That’s for wide approval and for good reason.
        For people more open to experimental treatments (especially when paying the additional drug out of pocket), the bar ought to be different. Somewhere on the level or ‘we have no idea if it will help but is unlikely to leave you worse than your current mono-therapy – at least biologically there is no reason why it would’.
        By now we know about a bunch of agents that might well fall under that umbrella – some of them even proven to lack interactions (*cough* metformin). Many are affordable, too.
        Now I do get part of the hesitancy – if everyone goes of and takes off label metformin/clemastine, we will never know if it does much of anything. But largely that seems not to be the reasons why neuros do not want to hear about it. It seems closer to ‘PwMS latching on to miracle cure du jour, need to stop them from taking snake oil’…

  7. Never mind cause. After a year of slow MS progression, a very smart GP sent me for a ton of bloodwork. I had both historical and currently active EBV. No illness symptoms – in fact, I never got sick with anything. It’s like my immune system was completely tied up trying to keep EBV in check. I had no neurological reserve. Only physical changes – fatigue, balance, worsening gait, increasing dependence on assistive devices. He put me on antivirals “just to see” and I regained my mobility, energy and functionality. I also ended up with a functional immune system and get symptoms of illness now. Since then, I have started Mavenclad, halved my antiviral and at some point will go off entirely.

    I think a full viral panel is essential for anyone showing “progression” – so many comorbid conditions take us down, and we have to be detectives and discern WHAT it is, because in many cases “progression” is manageable.

    1. Thanks for your report KC,

      could you share with us which antivirals are you taking?
      Maybe this could help many of our doctors, less smart than yours..

      1. Not a recommendation because I had to take double the normal dose to see a benefit. Acyclovir. He was a gp and this was all he felt comfortable prescribing. It’s not supposed to be helpful for EBV.

        However it was the difference between disabled and good function for me.

        Life as an experiment, n=1. 🤷‍♀️

      2. What dose did you take? Aciclovir comes in a variety of strengths from 200-800mg tables up to five times a day.

  8. I am right behind you. But HOW can we progress this?? What would it cost to be involved in a trial and treat going forward? If we can know £ and work back from there we have to find a way.

    It must be so frustrating for you … (as for PwMS, like me). Approaching 50 and need to halt progression.

    1. Ocrevus has a relatively safe transition profile. So…….. One could start with Ocrevus, then say they want to switch after 3-4 cycles to Teri. If phara will not fund the iTeri study, pwms are just going to have to do it themselves to prove efficacy. Neurologists are already throwing darts when tell us what drug to take.

  9. Theoretically, would you recommend an add-on antiviral to a a patient taking Ocrevus? I am very intrigued. How does this relate to someone who has had a IRT? In regards to HSCT or Lemtrada, does the treatment rid the body of EBV? Is HSCT superior to Lemtrada or Mavenclad of clearing the body of EBV? Would a test for EBV after one of these treatments come back negative? When I read about people who have had successful treatments with IRT (and claim remission) but later show progression, is this possibly due to reinfection of the cells with EBV?

      1. See MDs response to my question in the September 2020 Q&A. Short answer, they do not know, need a study to find out.

        I had to stop Ocrevus due to adverse reactions, so I decided to take Teri during b-cell repopulation and as a transition drug. Safe and may actually help me rid EBV. Using the lower dose in an effort to avoid side effects. I am monitoring my lymphocytes and EBV regularly, so I will keep the blog readers updated on my “single case” report. 😉 So far no major flair ups during the transition, but then again I just started to repopulate. Fingers crossed…..FYI, I had breakthrough lesions while on Ocrevus.

  10. I’ve lost so much to my ‘PPMS’, as have many people. I’m not moved by posts such as this any more, it’s like a self protective psychological reaction. I just shut off. I don’t want to ride the Hope and Despair rollercoaster any more. I’ll just go and make a cup of tea now, and have a homemade bread roll. I’ve not decided whether to put Marmite or honey on it…

  11. There is some light at the end of the tunnel, is there not ProfG? I see there is ATA188 in the pipeline. Did you not mention a HAART trial few days ago? Is Temelimab related to EBV? I also see significant mention of EBV and smouldering MS in some of the pharma brochures. Do you think there is some momentum gaining in this direction? My wife got diagnosed this year, I am asking these questions for my own peace of mind 🙂

  12. I’ve asked previously in the Q&A if after IRT’s those of us positive for ebv antibodies should consider being on some kind of antiviral to try and minimise risk of EBV reactivation? Is there any up u would suggest, or perhaps there is not enough evidence as yet

  13. Instead of a black swan it should read

    Groundhog: Anecdotal evidence we can’t ignore but we do due to lack of funding. Another year another post.

    Contact J.K. Rowling and see if she will donate in remembrance of her mother,

  14. 800 mg daily. I crashed if I tried to take less. Until year 1 month (?) 6 or 7 Mavenclad, when I reduced to 400 mg successfully. Still fine :).

  15. Dear professor Gavin Giovannoni,

    First and foremost I want to say thank youu for holding your grounds within the scientific community concerning the Epstein-Barr virus being the cause of ms. It must of been hard at times when people simply look away but there are people like me who are grateful for people like you. You give me hope for a cure.

    I wanted to give you some hope with the following study that should soon be published. Dr. Helen Tremlett is currently in her last few months of her study titled : Human immunodeficiency virus, antiretroviral drugs and multiple sclerosis risk (HIV-MS). Once her study is out she should be able to confirm that antiretrovirals reduce the risk of MS. This study if being funded by the Multiple Sclerosis Society of Canada.

    Perhaps you will have a better chance of getting funds for a clinical trial involving TAF to treat MS once her study is published. Her study should be finished either by january 1 2021 or april 1 2021. Perhaps you would be interested in participating in the virtual MS Connect conference happening this year from november 23 to november 28 I believe ? This conference will be hosted by the MS Society of Canada. Dr. Helen Tremlett should be there and maybe you could team up with her for initiating a clinical trial ( HAART ) if that could be of interest ?

    My question to you is what are the name of the researchers that have just received funding in the USA for starting a clinical trial involving HAART to treat MS ?

    I want to say thank you once again and have a great day Dr. Gavin Giovannoni 🙂

  16. I write these comments only to educate those new to this blog who will get their hopes high and tell family and loved ones there’s a light at the end of the tunnel and daughter I will be able to walk you down the aisle when you grow up and get married. Or son I will see you graduate and be there for your graduation ceremony. Read my lips. These and other articles like this will NEVER TRANSLATE to clinical practice Not because barts can’t convince other colleagues. They are stum because they won’t bite the pharma hand that feeds them. I suspect these articles are more to scare pharma into ensuring research teams are fully utilised and funded on long term treatments then engage in cure for research. READ MY LIPS. THERE WILL NEVER BE CURE FOR MS AS LONG AS THERE IS NO FINANCIAL BENEFIT FOR PHARMA. No money making company will cut its own throat for the betterment of society. It is better to have no hope then false hope. Come back 5 years from now, then 10, etc. The debate will still rage on.

      1. “Other opinions are available”
        Not here they’re not because you mouse 2 censor them.

    1. You are correct I suspect that pharma would rather manage than cure a problem and now MS is a problem if its success. If some one comes up with a cure, they will become pharma. You are wrong that pharma wont go there but the approaches have so far failed.

      “They are stum because they wont bite the pharma hand that feeds them”……Why on why does it always have to be about us, when you have a rant. You are so full of it (Yes I am fed up with the endless slures..Read the White Knight posts.

      P.S. Alemtuzumab may be a cure for those that take it early enough. Furthermore the best chance for an antigne-specific cure has been thrown away because the correct approach was not used and the trials failed….SH1 sticks and no-one will go there, especially because of the patent situation.

      1. Thanks MD. Again not read white night posts but sounds like a group that Donald Trump will ask to be on stand by during election night. Yes its not about you. I’m not having rant just pointing out realities of research. I guess I’m really talking about head of departments who have to balance department budgets and still be commercially viable as a entity and at the same time push for research that is likely to be funded and ensuring the survival of the department. My comments are not about good or evil, black or white. The world is a grey place and no one is truly fully sits on the the other side of the fence. Err unless your Donald Trump. But hey prove me wrong and I will be first to congratulate barts. But my gut instincts have rarely been wrong. I diagnosed myself with ms 3 years before doctors agreed.

      2. Hello MD, what are you referring to with the antigen specific therapy? I think I missed this one.

        I read the white knights story. Very nice description of the painful process. It makes clear that setting up a treatment is a crazy efforts for non pharma. But this is also a governance and government problem that makes it that difficult. It should be addressed in some ways by patients and patients associations pushing on governments.
        I thought about that story and I was wondering if it would make sense to join efforts internationally between MS teams and charities to build up a committee made of reputed academic and clinical scientists to define, prioritize and fund clinical trials. Relying on the funding of several charities it could be possible to fund larger studies sharing the economic burden, the workload and the risks between countries. In case of failure the losses are shared and the impact is mitigated. I think patients would contribute, for example they have to get routine MRI scans and they could be used for collecting data. I think patients would contribute to the cost of the study at least for part of routine testing. I do not know if the alliance on ppms is something like this but it could be extended to MS from a more general perspective.

        I would like to ask if it is possible for the barts ms team to make some kind of poster to explain their view of MS and of potential therapies that provides also info on the connections between the approaches and ideas. There are many many ideas on this blog and it is not easy to view the full picture of disease and therapies.
        I am thinking of something that shows how the many treatment ideas are connected. In this post we say we need anti viral and that sound ok but at the same time you are also trying to remove OCB or fully deplete b cells from CNS. It is easy to get lost. Something like profG slides but focused on the big picture instead of specific trials. Maybe it already exists and I missed it as well.

        Thank you

  17. The complete version of this study contains all (or most) the cases of HAART/MS studies till the day it was published, for those interested to learn about HAART.


    One might find that it is not as easy to pin the reason of why these drugs work, as only some have been found to have an effect on EBV. And you can not omit to mention the HERV implication as a possibility.

  18. Because biased science is bad science, the complete initial regimen of the patient was a combination
    of elvitegravir, cobicistat, emtricitabine, and TAF and the new regimen
    was changed to a two-tablet regimen containing raltegravir, emtricitabine,
    and TDF.
    A new MRI-scan was performed four months after
    the switch of HIV medication, showing one new gadolinium-enhancing
    lesion, a sign of new MRI disease activity occurring during the last
    months. Except for this single gadolinium-enhancing lesion, her MRI
    remained stable. Her clinical status has been unchanged after switching
    treatment, and she has not experienced new relapses or disability
    worsening. She did not become pregnant during the follow-up period
    and has continued with the two-tablet regime until now, without any
    additional disease-modifying therapy for her MS. She has still less MSrelated
    symptoms than when she used fingolimod.

  19. Yes, pharma may prefer to manage rather than cure… but no if the cure generates more revenue than the management of the disease. For example why Roche is doing the double dose trial? Double the dose higher the revenue and vit is still clear that it will not definitely halt progression maybe delaying it a little.
    Think of potentially curative approaches for several diseases that were launched in the past few years: short term treatments with extremely high prices and high success rates. Translate it to MS where disease management in terms of drugs, assistance and rehabilitation have a huge impact on healthcare systems sustainability. You will see that a cure would be convenient to be developed and priced high as it could be more cost effective than disease management. Consider also that if a cause is not found prevention is not possible therefore every year there will be patients filling up pharma pockets. The points are that pharma have lots of money but the amount is not unlimited, the development of a drug comes with a high risk of failure (MS is a field full off failures), development itself is high in costs. A pharma company will take the road only if at the end there is the shining light of money. Our world is run by investors and revenues that’s the way it works.

  20. What I’d like to know is how many of the anonymous members here are qualified in this area?

    To be honest, I thought Black Swan was a Thom Yorke song. But now I understand.

    Be kind.

  21. I was diagnosed with MS 13 years ago but have always had a very mild case. I have also was on Truvada from 2012-until early this year then switched to Discovy this year for HIV prevention. It would seem to me that if TDF or TAF has an impact on MS disease progression that you could find cases throughout the gay community of people that have been on these drugs for years either for HIV or HIV prevention and look how their MS has progressed. I wasn’t even on a DMT until about 2 years ago, and that was only started because it’s the standard of care.

    1. Unless you are one who has (anecdotal) documented issues with EBV impacting your course of MS.

      Not certain we can say “probably not”. Perhaps not every person’s experience .. but there are some.

      1. Recent study from Sanadaj, Iran looked for evidence of increased antibodies to EBV in MS patients in comparison to control population (something one would expect if EBV played a role in causing MS) and found: “There was no significant difference in the results of IgG antibodies against EBV in patients with MS and healthy controls.”


      2. 95% of the population infected with EBV, 100% with MS why would we expect a difference?

      3. In addition, there appears to be no correlation between EBV antibody titres and MS disease activity:
        “Increased levels of EBV IgG antibodies, including against EBNA-1…[was not] associated with an increased risk of CIS conversion to MS, or MS activity or progression over a 5-year follow-up.”


      4. again if every on had this it wont correlate….e.g. black hair in people from China does not correlate with MS even if it was the problem

      5. Even this paper that wants to prove EBV correlation, it only proves the opposite

        “he complete initial regimen of the patient was a combination
        of elvitegravir, cobicistat, emtricitabine, and TAF and the new regimen
        was changed to a two-tablet regimen containing raltegravir, emtricitabine,
        and TDF.
        A new MRI-scan was performed four months after
        the switch of HIV medication, showing one new gadolinium-enhancing
        lesion, a sign of new MRI disease activity occurring during the last
        months. Except for this single gadolinium-enhancing lesion, her MRI
        remained stable. Her clinical status has been unchanged after switching
        treatment, and she has not experienced new relapses or disability
        worsening. She did not become pregnant during the follow-up period
        and has continued with the two-tablet regime until now, without any
        additional disease-modifying therapy for her MS. She has still less MSrelated
        symptoms than when she used fingolimod.”

  22. I was diagnosed with glandular fever at the age of 16 and again at the age of 41. 18 months ago at the age of 69 I was diagnosed with with MS and was told by the specialist that there is no connection, but I am not convinced. I would value your opinion please.

    1. It is well known that EBV infection increases risk of M and it is well known that glandular fever increases that risk further…Obviously not too well known as your neuro doesn;yt know this

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