#PlainEnglish: Targeting the “virus factory” to stop MS activity

This is a #PlainEnglish version of this post.

We are trying out ‘translating’ some of the posts on the blog so they’re accessible and understandable to a wider audience.

Memory B cells and MS
We have been saying that the MS drugs which seem to work the best, appear to deplete memory B cells the most.

Memory B cells are cells that have helped your body to fight infection. A number of them stay dormant in the body and remember the infection. They can fight it off when the infection returns to the body. The problem is that they can sometimes attack the body, instead of attacking infections. They can create cytokines, “baddies” that can help other cells to create MS, or stimulate T cells to do the business.

In the past Prof G has called this idea the ‘Black Swan Theory’ (here, here and here). It’s when something unusual or highly improbable occurs, and has the potential to have an enormous impact. For MS, that means that instead of MS treatments targeting T-cells, they should instead target Memory B cells. It’s a game-changer, because it suggests MS may be caused by a virus that hides in the memory B cells. Although some treatments currently do deplete Memory B cells, MS is still primarily thought of as a T-cell disease.

Is MS caused by a virus?

Epstein Barr Virus (EBV) hides in Memory B cells. It shows itself every so often, when the T cells can kick its butt.

We’ve suggested that ocrelizumab – in targeting B cells, may actually be destroying a “virus factory”. Indeed we’ve said that all active MS drugs may be doing this. Is there evidence for this?

In a study done on treating EBV with rituximab patients in a DIFFERENT disease, those with the highest level of EBV showed the best response to therapy, compared to people who were so-called EBV negative.

But the results didn’t show 100% response to the drug. Why? And why is it that some B-cell-targeting drugs don’t stop MS activity fully? The treatment failure may be because the cells causing the failure are already in the brain and it is too late. In the study, the bone marrow was also not emptied by rituximab. Other studies show rituximab does not effectively deplete EBV in the lymph glands.

What does this mean for MS treatments?

Earlier in the week we suggested alemtuzumab may fail in many people after switching from fingolimod, this is because it traps white blood cells in the lymph glands and bone marrow and because alemtuzumab does not clear out the bone marrow (this is based on an animal study). Is the level of purging of the bone marrow and lymph glands by ocrelizumab going to be enough so it doesn’t to suffer the same fate as alemtuzumab after fingolimod treatment?

About the author

Rebecca Aldam


  • Rebecca – thanks. Easy to understand and nice plain English. Wish Mouse Doctor a happy retirement (or else you could share your writing skills with him).

    • Thanks Anon! So nice to hear that it's useful. We'll be working on more of these posts so spread the word!

      It is most definitely a collaboration. I'm just the translator; all credit to the original author 🙂

    • Great translation Rebecca, you're like the Google app for science 😉
      MD, please don't sulk, I absolutely love your posts they always make me smile and I'm learning stuff too. Particularly liked the journey from London to Leeds in this one 😀

    • Thank you Judy! I will be translating some more posts (hopefully doing a better job thank Google Translate?!?) Feedback is always welcome 🙂

  • So has anyone ever looked at whether Cladribine can clear the bone marrow the brain as a whole from the remnants of EBV?

    P.S.: I loved this publication, but I confess I'm a fan of the MD and NDG publications.

    • I dont think so, I did ask someone from Merck if they have did any monkey work (cladribine doesn't work on mice). I suspect all work is on hold to see if they get a licence.

    • This is very bad because we will not have that answer, whether or not the "EBV factories" are exhausted.

  • I'm wondering if you have any thoughts about the potential connections between the virus theory of MS and Valter Longo's work on fasting. I ask because it seems there is a logical connection between fasting rejuvenating the immune system by clearing out senescent immune cells, and latent EBV activating memory B cells. They've observed basically a 50% reduction in white blood cell count during fasts, followed by a return to normal in the weeks after the fast. There is also one study which showed positive results in MS patients. https://www.sciencedaily.com/releases/2016/05/160526151941.htm

    • You're so welcome Spodaddyo 🙂
      We're hoping to do some more of these Plain English posts. If you find something specific you'd like me to have a go at in the meantime, please let me know!



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