Good luck with the presentation, Prof G! Honestly, as someone with MS who is just fighting to survive each day, I don't think this stuff effects me personally. It would have to lead to a treatment that undoes the damage already done to me by MS and the NHS. And be available in my lifetime. And to someone in my socioeconomic position. I'm not optimistic 🤕
Might autoimmunity be triggered by a response to a virus?
So far we have lots of autoimmune diseases. No-one ever really bothers to find out what triggered them since, once triggered, they seem to carry on by themselves after the trigger is removed. At least as far as anyone can tell...
With MS there's a possibility that cycles of EBV flaring and cycles of MS flaring are simultaneous and could even be causal. Certainly, as you mention, Atara are looking at "what happens if we find a way to break this potentially causal link?". Similarly, a few more intrepid (desperate?) MS patients are finding ways to routinely obtain drugs such as Tenofovir which may reduce EBV levels and potentially lead to halt in progression and even possibly reversal of some damage.
Whilst this would never be able to repair full ataxia, never say never...
https://www.bbc.com/news/science-environment-65689580 - "The act of walking trains their muscles and has restored a degree of movement when the system is turned off, suggesting that damaged nerves may be regrowing."
May 25, 2023·edited May 25, 2023Liked by Gavin Giovannoni
A billion dollar question - how much would it cost the pharma companies in revenues if it is proven MS is due to a virus rather than an autoimmune disease?
May 31, 2023·edited May 31, 2023Liked by Gavin Giovannoni
Dear Prof. G,
you are mentioning that the cervical lymph nodes are of special interest in reducing EBV/ MS interactions. As Ofatumumab s.c. injected in the lower extremities seams to be distrubuted also by the lymphatic vessels - wouldn't it be interesting to inject it in the buccal region s.c. so it is drained via the cervical lymph nodes? Furthermore, if EBV clearing of cervical nodes is of special interest - wouldn't it be intersting to explore CD19-Ab s.c. in the buccal and/or nuchal regions s.c. to reduce the load of EBV infected B-cells and plasma cells from the cervical lymph nodes?
Prof G, you are the one to lead this discussion! Below is how I've been describing the options to treat EBV. You did not include option 3, restor immune tolerance to MBP. Does this not seem feasible to you?
Treating Epstein Barr (EBV) as a cause of MS is planned or currently underway in multiple trials. The approaches can be grouped into four categories.
1) Diminishing the viral load of EBV with antiviral or antiretroviral treatments with currently available drugs, which is the subject of this profile. None of these currently approved drugs are optimal for EBV so the question is, can they fill a stop-gap role while more effective therapies are designed specifically for EBV? Also, May 2023 the Immunic trial of Vidofludimus Calcium reported a strong antiviral effect against EBV.
2) Selectively removing EBV-infected B cells with modified T cells (e.g. ATA188 by Atara; Imotope peptide by Imcyse).
3) Rather than directly remove EBV as in the first two approaches, restore regulatory and inflammatory T-cell balance, to induce immune tolerance to MBP. There are currently 10 trials to correct intolerance to myelin basic protein due to molecular mimicry caused by EBV (e.g. ANK-700 peptide, LPX-TI641 activates the Tim3 and Tim4 receptors, to boost expansion of Tregs, and multiple mRNA therapeutic vaccines).
4) Combing one of the first 3 options with remyelination or neurodegenerative repair therapies, some of which are already showing positive results in trials (e.g. MSC stem cells, CNM-Au8 Nanocrystalline Gold, NVG-291 and others)
I’m sincerely hoping that your approach is taken seriously and there will be funding. I admit what immediately came to mind was what Stephen voiced. Stick to it!! Best regards, Prof G with your presentation.
This week's article was very hard to follow for a ley person like me. A single silver bullet has long since been ruled out for MS leaving the collusion of one or more factors being likely.
* Is EBV a catalyst? Some have suggested covid has triggered MS too? Both viral. Why does EBV activate in some people to cause IM? Why did Covid-19 kill a small number of people who fell outside the high-risk groups?
* And what of the role of stress testing? By putting the body under undue load e.g. childbirth, stroke, serious injury appears to make the body vulnerable to attack.
As you say, big data may provide the answers and join the threads together because they seem disparate at the moment.
Good luck with the presentation, Prof G! Honestly, as someone with MS who is just fighting to survive each day, I don't think this stuff effects me personally. It would have to lead to a treatment that undoes the damage already done to me by MS and the NHS. And be available in my lifetime. And to someone in my socioeconomic position. I'm not optimistic 🤕
Is there any possibility of doing radiolabled acyclovir imaging (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7125728/) to see if EBV lytic activity corresponds to MS lesion location or disease activity?
Might autoimmunity be triggered by a response to a virus?
So far we have lots of autoimmune diseases. No-one ever really bothers to find out what triggered them since, once triggered, they seem to carry on by themselves after the trigger is removed. At least as far as anyone can tell...
With MS there's a possibility that cycles of EBV flaring and cycles of MS flaring are simultaneous and could even be causal. Certainly, as you mention, Atara are looking at "what happens if we find a way to break this potentially causal link?". Similarly, a few more intrepid (desperate?) MS patients are finding ways to routinely obtain drugs such as Tenofovir which may reduce EBV levels and potentially lead to halt in progression and even possibly reversal of some damage.
Whilst this would never be able to repair full ataxia, never say never...
https://www.bbc.com/news/science-environment-65689580 - "The act of walking trains their muscles and has restored a degree of movement when the system is turned off, suggesting that damaged nerves may be regrowing."
A billion dollar question - how much would it cost the pharma companies in revenues if it is proven MS is due to a virus rather than an autoimmune disease?
Dear Prof. G,
you are mentioning that the cervical lymph nodes are of special interest in reducing EBV/ MS interactions. As Ofatumumab s.c. injected in the lower extremities seams to be distrubuted also by the lymphatic vessels - wouldn't it be interesting to inject it in the buccal region s.c. so it is drained via the cervical lymph nodes? Furthermore, if EBV clearing of cervical nodes is of special interest - wouldn't it be intersting to explore CD19-Ab s.c. in the buccal and/or nuchal regions s.c. to reduce the load of EBV infected B-cells and plasma cells from the cervical lymph nodes?
What are your thoughts?
Yours sincerely,
Paul
Prof G, you are the one to lead this discussion! Below is how I've been describing the options to treat EBV. You did not include option 3, restor immune tolerance to MBP. Does this not seem feasible to you?
Treating Epstein Barr (EBV) as a cause of MS is planned or currently underway in multiple trials. The approaches can be grouped into four categories.
1) Diminishing the viral load of EBV with antiviral or antiretroviral treatments with currently available drugs, which is the subject of this profile. None of these currently approved drugs are optimal for EBV so the question is, can they fill a stop-gap role while more effective therapies are designed specifically for EBV? Also, May 2023 the Immunic trial of Vidofludimus Calcium reported a strong antiviral effect against EBV.
2) Selectively removing EBV-infected B cells with modified T cells (e.g. ATA188 by Atara; Imotope peptide by Imcyse).
3) Rather than directly remove EBV as in the first two approaches, restore regulatory and inflammatory T-cell balance, to induce immune tolerance to MBP. There are currently 10 trials to correct intolerance to myelin basic protein due to molecular mimicry caused by EBV (e.g. ANK-700 peptide, LPX-TI641 activates the Tim3 and Tim4 receptors, to boost expansion of Tregs, and multiple mRNA therapeutic vaccines).
4) Combing one of the first 3 options with remyelination or neurodegenerative repair therapies, some of which are already showing positive results in trials (e.g. MSC stem cells, CNM-Au8 Nanocrystalline Gold, NVG-291 and others)
I’m sincerely hoping that your approach is taken seriously and there will be funding. I admit what immediately came to mind was what Stephen voiced. Stick to it!! Best regards, Prof G with your presentation.
This week's article was very hard to follow for a ley person like me. A single silver bullet has long since been ruled out for MS leaving the collusion of one or more factors being likely.
* Is EBV a catalyst? Some have suggested covid has triggered MS too? Both viral. Why does EBV activate in some people to cause IM? Why did Covid-19 kill a small number of people who fell outside the high-risk groups?
* And what of the role of stress testing? By putting the body under undue load e.g. childbirth, stroke, serious injury appears to make the body vulnerable to attack.
As you say, big data may provide the answers and join the threads together because they seem disparate at the moment.