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Does EBV cause MS?

Discussion in 'Other Health News and Research' started by Ecoclimber, Feb 12, 2014.

  1. Ecoclimber

    Ecoclimber Senior Member

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    In my previous thread located here: http://forums.phoenixrising.me/index.php?threads/immunotherapy-against-ebv-targeting-ebv-infected-cells-using-immunotherapy.28058/ , I mentioned the discussion of Immunotherapy against EBV in the treatment of MS on a research blogsite for MS at Barts London School of Medicine and Dentistry. Since it is of interest and discussion to many in the ME/CFS community, the continuing role of EBV, B-Cells, autoimmune diseases and the UK's rituximab study, I found this lively discussion on the same blogsite concerning EBV role in MS and autoimmune diseases.

    It has sometimes been stated that researchers have the tendency to narrowly focus or acquire 'tunnel vision' when it comes to their own specific area of research and thereby avoid making paradigm shifts from established norms. It is refreshing though to find researchers who will buck the system, think outside the box and push the envelope into other possibilities.

    One never knows whether an area or knowledge of research into a specific disease such as MS could cause a connective pathway to other diseases, specifically in the autoimmune category which ultimately could lead to a possible breakthrough in ME/CFS. As the good professor stated in the story of the Black Swan.

    Permission to Repost:

    Guest Post: Professor Michael Pender

    Professor Michael Pender explains how anti-EBV cell therapy works in MS. #MSBlog #MSResearch
    "At the request of one of you and following on from his recent publication on treating EBV by transfer of virus killing T cells we asked Prof. Michael Pender from Australia to give you more details on his group's work."

    Professor Michael Pender graduated from The University of Queensland in 1974 with First Class Honours in Medicine and a University Medal. Over the next six years he trained as a physician and neurologist at the Royal Prince Alfred Hospital and St Vincent's Hospital, Sydney, and became a Fellow of the Royal Australasian College of Physicians in 1981. During his clinical training he developed a keen interest in multiple sclerosis which has continued since then.

    After completing clinical training in neurology, he commenced research on experimental autoimmune encephalomyelitis under the supervision of Professor Tom Sears at the Institute of Neurology, Queen Square, London. In 1983 he was awarded a PhD from the University of London and Queen Square Prize for Research. From 1984-1986 he continued this research as a Research Fellow at the John Curtin School of Medical Research, Australian National University, Canberra, in the Department of Experimental Pathology chaired by Professor Peter Doherty, Nobel laureate. In 1987 he was appointed Senior Lecturer in the Department of Medicine, The University of Queensland, at the Royal Brisbane Hospital. In 1989 he was awarded a Doctorate of Medicine from The University of Queensland for research on experimental autoimmune encephalomyelitis and was promoted to Reader in Medicine. In 1995 he was promoted to Professor of Medicine (Personal Chair), The University of Queensland. He also held the position of Director of Neurology, Royal Brisbane and Women's Hospital, from 1992-2005. He is Director of The University of Queensland Multiple Sclerosis Research Centre and an Honorary Senior Principal Research Fellow at the QIMR Berghofer Medical Research Institute, and directs the Multiple Sclerosis Clinic at the Royal Brisbane and Women's Hospital. In 2006 he was awarded the Multiple Sclerosis Australia Prize for Multiple Sclerosis Research - 'For outstanding commitment and dedication to research into the cause and cure of Multiple Sclerosis in Australia'. In 2011 he received the John H Tyrer Prize in Internal Medicine, The University of Queensland, for research in the field of Internal Medicine.

    Professor Pender writes:
    A large body of evidence indicates that infection with Epstein-Barr virus (EBV) has a role in the development of multiple sclerosis (MS).

    EBV infects B cells and plasma cells, the white blood cells that make antibodies. Once a person is infected with EBV, they carry the virus in their B cells for the rest of their life.

    Normally the number of EBV-infected B cells is kept under tight control by the immune system especially by CD8+ T cells, which kill the infected cells.

    In 2003 I published a new theory in Trends in Immunology proposing that chronic autoimmune diseases such as MS and rheumatoid arthritis are caused by uncontrolled EBV infection leading to infection of autoreactive B cells, which accumulate in the organ affected by the autoimmune disease.

    I proposed that MS was caused by the accumulation in the brain of EBV-infected autoreactive B cells which produce anti-brain antibodies and also provide survival signals to autoreactive T cells that would otherwise die in the brain by apoptosis (programmed cell death).

    The theory made predictions which have subsequently been verified, namely: the presence of EBV-infected B cells in the brain in MS; a beneficial effect of rituximab which kills B cells, including EBV-infected B cells; decreased CD8+ T cell immunity to EBV in MS; and EBV infection of autoreactive plasma cells in the joints of people with rheumatoid arthritis.

    It also predicted that boosting CD8+ T cell control of EBV by vaccination or by adoptive immunotherapy would prevent and successfully treat chronic autoimmune diseases.
    EBV-specific adoptive immunotherapyinvolves growing T cells from the blood in the laboratory with an EBV vaccine to retrain the cells to be potent killers and then returning them to the patient by intravenous infusion.

    This treatment was developed by Professor Rajiv Khanna of the QIMR Berghofer Medical Research Institute in Brisbane to treat patients with EBV-related malignancy and does not require the use of any drugs.

    Professor Khanna and his team have successfully used this therapy to treat EBV-related metastatic nasopharyngeal carcinoma.

    This EBV vaccine expresses parts of three EBV proteins, which are crucial in allowing EBV-infected B cells to multiply and mature into memory B cells and plasma cells capable of producing large amounts of antibody.

    As it happens, Francesca Aloisi’s group have shown that these same three EBV proteins are the main EBV proteins present in the brain-infiltrating EBV-infected B cells in MS.

    EBV-specific adoptive immunotherapy has not previously been used to treat people with MS or any other autoimmune disease.

    Because we were concerned that the therapy might aggravate inflammation in the brain and actually worsen MS, we reduced the initial dose of T cells to 25% of the dose used by Professor Khanna to treat EBV-related malignancy.

    We then gradually increased the dose over the next three infusions, which were administered at fortnightly intervals. The first recipient was a 42 year old man with secondary progressive MS. The treatment had no adverse effects and within 2 weeks the patient began to experience clinical improvement.

    This was followed by further improvement, with a reduction in fatigue and painful lower limb spasms, an improvement in cognition and hand function, and increased productivity at work.

    These improvements were sustained up to the time of the latest review, 21 weeks after the final T cell infusion, when neurological examination demonstrated increased movement of his legs.

    There was also reduced disease activity on his MRI brain scan and reduced antibodies in the cerebrospinal fluid.

    We believe that the beneficial effects of the therapy are due to the killing of EBV-infected B cells in the brain by the transferred CD8+ T cells.

    The beneficial effect of boosting immunity to EBV by this treatment highlights the importance of impaired immunity to EBV in the development of MS. A clinical trial is now needed to determine safety and therapeutic efficacy across the clinical spectrum of MS.



    The lively discussion follows on their site in the comment section:

    Eco
     
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  2. Daffodil

    Daffodil Senior Member

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  3. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Ebv keeps popping up in different research but pushed aside by many as benign. Maybe this will start to change this thinking and maybe people with mono treated more aggressively than just rest??
     
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  4. rosie26

    rosie26 Senior Member

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    I really don't get the EBV - I know I have never had mono - I would have been sick enough to remember it and two tests I have had done were negative. I can see it confusing some MS sufferers in the comments section as some of them probably don't have EBV either.

    So EBV may worsen symptoms of MS in those who do have EBV with their MS.
    Maybe those who have EBV in ME are more likely to be vulnerable to lymphoma than those who do not have EBV in ME ? I don't know if I am reading this right.?
     
  5. August59

    August59 Daughters High School Graduation

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    That same group from Australia has also made another novel discovery about EBV, which has long been understood to attach to the CD21 receptor on semi-mature and mature B-cells. However there are a few humans that are void of the CD21 receptors on B-cells, but they are still infected and carry the EBV. They discovered that the EBV can attach to the B-cells at another receptor site as well named CD35 and all humans have this receptor!

    Here is one link to the study finding the new receptor binding site for the EBV and this attachment location, if I read it right, associates this binding receptor site as being associated with malaria. I'm also not sure if it was the same group that made this discovery or not.

    http://www.medicalnewstoday.com/releases/256778.php

    There is another thread that was discussing this and other research findings and here is its link.

    http://forums.phoenixrising.me/inde...-using-immunotherapy.28058/page-2#post-428155

    What I wonder, to an extent, is what if EBV can attach twice to the same B-cell at each receptor? I could see where this might be a factor in the development of a compromised immune system and also making it harder to treat.
     
    Last edited: Feb 12, 2014
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  6. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    I just dont think the current testing methods used in commercial labs is very accurate, I cant back this up but there definately is a group who are affected by ebv, maybe its a seperate illness but can cause other illness such as ms etc?? Also testing is mostly in the blood, maybe these infections are in different tissue, muscles, brain, nerves etc??
     
  7. anciendaze

    anciendaze Senior Member

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    As I've pointed out at other times and places, the research by Dr. Carmen Sheibenbogen indicates EBV can cripple highly-specific immune responses to itself, and can replicate without killing cells, (lytic replication). If the virus is able to replicate during phase 1 latency and exploit cell mitosis to infect cells generated during clonal expansion, and if response to EBNA-1 is crippled, any measurements of viral load based on immune response could be wildly inaccurate. Viruses such as HIV and Hepatitis C virus do, in fact, wreck specific immune response to themselves.

    This kind of behavior has long been seen in chronic bacterial diseases like TB. If you don't catch the infection soon after onset, a person dying of miliary TB can return a false negative to a test based on tuberculin response.
     
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  8. natasa778

    natasa778 Senior Member

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    could this offer some sort of very basic and crude explanation of the difference/s btw MS and ME - in MS those cells would accumulate in the CNS and the brain itself, whereas in ME it would be primarily in the the ANS and the periphery, gut lining etc?

    There is also the question of bone marrow and stem cells being infected, right? If they are infected then we would not expect rituximab to work for those patients, except maybe bring short-lived improvements?
     
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  9. Iquitos

    Iquitos Senior Member

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    This article shows the value of researchers and doctors graduating from the reductionist view: that there is one cause for each problem and one magic-bullet solution, to an understanding of synergy.

    When they begin to understand synergy, both the synergy of the microbes and the synergy of treatments, we may begin to get somewhere in understanding and treating mecfs and a lot of other complex diseases.
     
  10. anciendaze

    anciendaze Senior Member

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    Iquitos, people denounce reductionism without even understanding the prime example where it worked. Isaac Newton did break very complex dynamical problems down to treat entire planets and stars as point masses seen at instants of time. What people seem to have overlooked is that he invented the calculus to put the pieces back together, to construct the long-term behavior of solid bodies from point masses and moments of time. Reductionist medicine has never figured out how to put things back together at all. If your heart, lungs, liver, kidneys, stomach and gut check out separately, any remaining problems must be imaginary.

    I've said it before, and I'm sure I will say it again, the immune, endocrine and nervous systems are extremely complicated dynamical systems, and they are being approached by people who don't seem to think dynamic behavior is important until things go way beyond arbitrary bounds. This is like a mechanic telling you your automobile suffers from chronic water deficiency and needs periodic supplements to keep running. He is missing an important point about how it reached that state. Failure need not be a sudden crack, it can be a continuous process. When it is, you have the chance to detect this and intervene before it becomes irreversible.
     
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  11. A.B.

    A.B. Senior Member

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    Speaking of reductionism: I find it ironic that the same camp that likes to dismiss science as being reductionist, is often also the one that reduces everything to "incorrect beliefs and behaviour" or "positive thinking".
     
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  12. August59

    August59 Daughters High School Graduation

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    I certainly don't have the knowledge to even give you an educated guess. I can only say that there still a few scientist that are not through with researching EBV in the least. Many in the research field felt like when EBV was found to cause "mono" that was the end of it for them.

    I believe when these remaining scientist or researchers are finished or satisfied with what they have found that there will be a pretty extensive list of diseases and cancers that are directly associated with the EBV, but also there some diseases and cancers that will be caused or fostered in some way by the EBV.

    I don't think there has been a year since 2000, or even before, that has not produced new replicated evidence of how powerful and elusive this virus is. The term "elusive" being a very strong trait of EBV, but much of this research that has shown how powerful this virus can be is due to advances in research and pathogen discovery technology.

    My answer to your question is "It is very possible!!"
     
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  13. August59

    August59 Daughters High School Graduation

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    I don't think many of them are very accurate either. I believe most of it comes from the fact that a research lab is not under time restraints to process samples, so they are meticulous in their findings. Then there comes the problem with commercial labs that use very high throughput and testing methods (Labcorp, Quest, Spectrum, Solarus plus you have some very large practices that have their own in-house high throughput equipment that are terribly inaccurate except for very basic analysis) that have been reduced in accuracy due to a time "and cost" attitude because insurance is not going to pay a very high price if they can help it.

    One of the fields of "lab testing" that is very prone to inaccuracies in both directions of detection is "drug screening" as there are a lot of false positives and false negatives, but these test are very cheap for the most part. It is causing potential employees to not be hired, present employees are fired, commercial vehicle (truck drivers) are being fired when they are clean and some are left on the road when they are high as a kite, as patients in "Pain Management" practices are being kicked out of because of many false positives, even when many "positives" are sent for GC/MS analysis which is suppose to be the holy grail as most high throughput labs don't have qualified technicians to interpret GC/MS analysis. This last information I actually received in person from a lab doctor at the Mayo Clinic. He said they are close to the best along with several other teaching and research institutes and they are not over 95% accurate in their most reliable test. They have had contaminated collection cups, people on herbs that have been laced with illicit drugs. The worst clinical problem was patients that are taking oxycodone for pain and they are tested by their "pain clinic" and it comes back negative about 50% of the time, when in fact it is positive. Many of these patients are terminated for treatment because they are accused of selling their medication they were prescribed because "negative" test are not sent for a 2nd analysis by GC/MS verification because it is expensive.

    There is a study out now that has shed doubt on the accuracy of high throughput "deep sequencing assays" due to a lot of cross reactivity being found. This worries me a little because I believe this what Dr. Lipkin is using in some of his testing. I would hate to think that there are some of his samples that are actually positive for a virus/pathogen and it is being missed due to high throughput analysis. It would take many years to have a 200 sample study, that is looking for several hundred viruses and bacteria, without using a high throughput assay to do the analysis though.

    It would be nice to see 15 patient samples and 15 healthy control samples verified by thorough analysis by Dr. Montoya at Stanford since he would have the resources to them fairly quickly (I would hope!!).

    I do think high throughput testing will get better due to technology advancing so quickly as it has in the last 5 to 10 years. I believe it was Dr. Bariniuk that stated that 10 years ago he was not able to sample spinal fluid from 3 different sample pools and differentiate between the various groups and find out which proteins were in common and the ones that were specific to the different groups and that they are close to getting to where the proteins can be positively identified quickly.
     
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  14. Ecoclimber

    Ecoclimber Senior Member

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    Another article on the subject is located here:
    Exploiting the EBV-MS Link to Quell Secondary Progressive Disease

    Adoptive immunotherapy targeting EBV-infected B cells was safe and improved symptoms in a case study of secondary progressive MS
    Ricki Lewis, Ph.D.

    Adoptive immunotherapy that targets the immune system response to EBV-infected B cells helped one patient with secondary progressive MS, as reported February 3 in Multiple Sclerosis Journal (Pender et al., 2014). The response provides the proof of concept for a clinical trial, according to lead author Michael P. Pender, M.D., Ph.D., and colleagues from The University of Queensland.

    Whether the relationship between prior infection with Epstein-Barr virus and MS is cause or effect remains unclear. EBV is present in 90% of the healthy adult population, yet in 99% of people with MS (Bagert, 2009).
     
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  15. natasa778

    natasa778 Senior Member

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    Pender's reply to questions on the blog

     
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  16. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    i was hanging around an ms site for a short time awhile back. There were a few ms patients trialling valtrex and finding symptom improvement. Just abit more evidence to this thread.
     
  17. Daffodil

    Daffodil Senior Member

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    I just assumed celebrities with CFS were getting adoptive immunotherapy for EBV and were able to function normally.....a rumor I heard long ago.

    it would be very costly, I think.

    Didn't the Germans find a new kind of latent EBV that is pumping out proteins but not actually replicating?

    Isn't this the sort of thing that Lerner has been saying all along? Although I am not sure why he prescribes Valtrex if that targets only the late stages of replication.

    Maybe if we had had adoptive immunotherapy when we were first infected, we would not have gone on to develop autoimmunity.
     
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