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The Charcot Project

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    The Charcot Project

    The Charcot Project will investigate the possibility that MS is caused by a virus. Simple, yet the implications are profound. Because if true treatments for MS would be radically altered.

    For years it was thought that stomach ulcers were caused by stress, foods, etc. The idea that stomach ulcers might be caused by bacteria was laughable to some, and pretty much disregarded by everyone else. Then someone purposefully infected himself with bacteria, got an ulcer, treated himself with antibiotics, got rid of the ulcer and shocked the medical community. Conventional approaches to disease treatment can get relegated to the trash heap overnight when significant discoveries are made.

    Those who want to know more about the Charcot Project may do so by viewing an introduction of it on YouTube at

    IMHO, it is unlikely any of the major drug companies currently making money from expensive MS treatments will spend any effort looking for what Charcot Project seeks… a viral cause for MS and an effective viral treatment for it. I wish them Godspeed.

    I found the YouTube video outstanding. Kind Regards.

    Thanks for posting this. I found the video compelling. Dale
    Dale in NC, dx'ed 2000, now SPMS


      I also have found information mentioned above as very helpful. thanks.


        Potential to turn the MS treatment world on its head!

        Good news about an Anti-Viral Trial in Multiple Sclerosis

        Estimated Study Completion Date: August 2014
        Raltegravir (Isentress) Pilot Study in Relapsing Multiple Sclerosis (INSPIRE) Identifier: NCT01767701

        "The purpose of this study is to determine whether raltegravir (an anti-viral medication) is effective in preventing progression of relapsing remitting multiple sclerosis as determined by gadolinium- enhanced MRI.

        Detailed Description:
        There is accumulating research evidence that Human Endogenous Retrovirus (HERV) and herpes viruses (in particular Epstein-Barr Virus) are involved in the pathogenesis of multiple sclerosis. People with active MS have higher levels of HERVs than people either without MS or who have other neurological conditions. It has been shown that HERVs may produce neurotoxic proteins/antigens associated with MS activity and disease progression.

        This is the first clinical trial investigating the hypothesis that the antiretroviral drug raltegravir may suppress HERV activity and ameliorate progression of relapsing remitting MS. Raltegravir is an integrase inhibitor which blocks retroviral replication. A recent experimental study suggests that raltegravir may also be active against herpes viruses.

        Eligible participants (see Inclusion/Exclusion Criteria) will be observed for 3 months having monthly brain Gadolinium enhanced MRIs and blood/urine/saliva sampling (baseline). Then they will be treated with raltegravir (one 400mg pill taken twice a day) for 3 months. During treatment period participants will continue to have monthly MRIs and blood/saliva/urine sampling.

        Participants will have monthly clinical and neurological examinations and they will complete questionnaires assessing response to treatment. Participants will have screening and study visits at The Royal London Hospital, Whitechapel. Monthly MRIs will be performed at the Institute of Neurology at Queens Square, London."


          This seems to be very interesting news. I wonder how this 'anti-viral' drug has been used before. I am sure that the drug company that manufactures it wants to get it approved for the MS community to use, regularly. I wonder what the side effects are.


            There is information about Merck’s anti-viral drug raltegravir available online, Jerry.

            The following link should be posted in this thread; it deals specifically with a virus which shows up at the crime scene too often not to be connected with MS, IMHO.

   I have no idea why this link does not always work but if it doesn't you can Google "Multiple Sclerosis and EBV: Relapsing Together" and find it.

            One section of the June 12, 2013 article asked:

            Could There Be a Viral Trigger for MS?

            "The role of EBV as a potential trigger for multiple sclerosis has long been debated. Whether it—or any virus—directly causes the disease or creates a “perfect storm” situation whereby the immune system, in trying to eradicate the virus, goes haywire and mistakes myelin proteins as the enemy, is unclear.

            According to Dr. Steven Jacobson..., it's important to note that "While EBV may be one of the triggers in MS...what triggers reactivation in one person may not in another." He told Healthline that MS is not a disease with a single, defined, viral trigger like AIDS, for example, which is triggered by the HIV virus.

            “The results [of this study] do not answer the question of whether EBV dysregulation is a consequence or cause of MS," said Dr. Tom Ech..., "but (the results) suggest a link between EBV reactivation, antiviral immune response and disease activity during the relapsing-remitting stage of MS.”

            The results of this study suggest that the ebb and flow of EBV as it cycles between dormant and active phases could set the stage for the reactivation of MS. This has led to the hypothesis that RRMS could be controlled with antiviral drugs that keep EBV in check. However, many more studies will be required to prove or disprove this theory."


              The Primate EAE Model Points at EBV-Infected B Cells as a Preferential Therapy Target in Multiple Sclerosis

              Published online 2013 June 13.


              Here is a newly published study in which the animal model of MS, experimental autoimmune encephalomyelitis (EAE) involved primates (marmosets) rather than typically used mice. It is my understanding that they used marmosets because they are one of the few species other than humans which can be infected by EBV (Epstein Barr virus).

              The full text is available by clicking the link below. IMO, it adds considerable evidence to the premise that MS has a viral component. Quote, “In conclusion, we propose that two herpes viruses may be implicated in the pathogenesis of MS.”

              The article suggests, “The therapeutic perspective and testable hypothesis following from this postulate is that therapeutics specifically targeting EBV-transformed B cells are a safe and effective treatment for MS.”

              But I’m getting ahead, be sure to check out the entire article or perhaps read the selected passages below. Currently, the most effective FDA approved MS treatment is Tysabri (natalizumab). Hopefully, the near future will see other just as effective monoclonal antibody treatments w/o the PML risk. And, possibly treatments based on dealing with EBV and CMV (cytomegalovirus).

              “The remarkable clinical efficacy of anti-CD20 monoclonal antibodies (mAb) in relapsing-remitting multiple sclerosis points at the critical involvement of B cells in the disease. However, the exact pathogenic contribution of B cells is poorly understood. In this publication we review new data on the role of CD20+ B cells in a unique experimental autoimmune encephalomyelitis (EAE) model in common marmosets (Callithrix jacchus), a small-bodied neotropical primate.”

              “Therapeutic mAbs that target both the T- and B-cell arms of the autoimmune attack show promising effects in RRMS. Examples are alemtuzumab... natalizumab... selective depletion of B cells via mAbs against the B lineage specific surface marker CD20 (rituximab, ocrelizumab, and ofatumumab) proved remarkably effective in the induction of long-lasting suppression of lesion activity and clinical relapses (Barun and Bar-Or, 2012).”

              “There is a vast body of literature data supporting the association of EBV infection with MS susceptibility (Christensen, 2007; Lunemann and Munz, 2009; Pender, 2011) but the underlying mechanism(s) remain poorly understood.”

              “The marmoset model thus supports the possibility that MS susceptibility may be associated with two herpes viruses, namely EBV (Epstein Barr virus) and CMV (cytomegalovirus). What could be the underlying mechanism? During the co-evolution with their natural host, CMV and EBV have developed an elaborate repertoire of strategies to avoid detection by the immune system.”

              “These findings support an important pathogenic role of CD20+ B cell in MS, especially of the subset infected with EBV.”

              The closer research comes to discovering a cause, the closer we are to safe, effective treatments or even a cure for MS. This study goes a long way to further establish a link between virus and MS, I believe. The study found monoclonal antibodies targeting B cells infected by Epstein-Barr virus were effective treating EAE an animal model of MS in marmoset primates. In my opinion, highly effective MS treatments will follow this research.


                Human endogenous retroviruses (HERV) are not viruses which you pick up; they are viruses which are part of your DNA. We are all born carrying HERV from our ancestors. 5% to 8% of our DNA is viral. The study below states,

                “Human endogenous retroviruses (HERVs) constitute 5 to 8% of human genomic DNA and have been detected as transcripts and proteins in the central nervous system (CNS) and peripheral blood, frequently in the context of neuroinflammation…We found a 4-fold increase in extracellular HERV-Fc1 RNA titers in patients with active MS compared with healthy controls (P < 0.001). These findings strengthen the link between HERV-Fc1 and the pathology of MS.”

                IMO, this study, “Expression of HERV-Fc1, a human endogenous retrovirus, is increased in patients with active multiple sclerosis” strengthens the idea that MS is an autoimmune reaction to viruses (HERV) in our DNA, usually latent, which have become active.

                A human trial based on this concept is being organized presently as identified in my previous post 7-2-13.


                  Tonsillitis and EBV in MSers.

                  Selected quotes from research presented by:

                  “Results: We identified 33 case–control studies, involving 27,373 multiple sclerosis cases and 211,756 controls. There was a statistically significant association between tonsillectomy… and the subsequent risk for developing multiple sclerosis.

                  Several theories linking tonsillectomy to MS risk have been postulated over the years. Meurman and Wising proposed tonsillectecomy as a possible risk factor for MS in that an upper respiratory tract infection may trigger MS or that a locally deficient immune system may facilitate the invasion of an etiologically relevant, infectious agents.

                  Tonsillectomy may leave sufficient lymphoid tissue adjacent to the central nervous system to instigate the exaggerated immune response seen in MS. Poskanzer (1965) was particulary interested in examining tonsillectomy and MS risk at it predisposes to the development of neurological complications in poliomyelitis, another infection that is much more widespread than is suggested by its neurological manifestations.

                  Of particular interest is the association between recurrent tonsillitis and EBV infection and reactivation.

                  Krone and collegues postulate that these findings reflect a dysregulation of immune function as a consequence of the development of the disease. They assert that immune dysregulation in MS is likely to be an early event preceding the onset of MS disease by many years or even decades.

                  It is likely that the elevated antibody concentrations do not directly cause MS but rather reflect a shift in patterns of immune reactivity away from protection towards enhancement of the risk of disease. These authors suggest that studies on MS-associated infectious agents could lead to the identification of specific antigenic determinants involved in the generation and maintenance of immune dysregulation.


                  This result of this meta-analysis suggests a statistically significant and clinically important increased risk for developing MS in those with tonsillectomy and appendectomy at ≤ 20 years of age. Despite this significant finding, this in no way suggests or demonstrates causality, in that epidemiological studies can only provide etiological clues at best.”


                    Antiretroviral medicines may curb MS, why?

                    Study published Aug 2013 titled:

                    Endogenous retroviruses and multiple sclerosis–new pieces to the puzzle


                    “We speculate that endogenous retroviruses may activate the innate immune system in a variety of ways, involving the host proteins... Observations in HIV-positive patients suggest that antiretroviral drugs can curb MS...”


                      Another piece of the puzzle suggesting infection as one of the triggers for MS

                      Bacterial Toxin May Trigger Multiple Sclerosis


                      "C perfringens B is found in soil and is not normally present in humans. It can live the gastrointestinal tract of grass-eating animals, where it can grow fast and make a toxin that causes neurological symptoms. In humans, who have a linear GI [gastrointestinal] tract, it does not grow well. Our hypothesis is that in some environmental conditions, this bacterium takes up residence in the human gut and makes this toxin."

                      Clostridium is a bacterium having 5 types, A, B, C, D, and E which are identified by the toxins they produce.

                      What makes this all so interesting is that Epsilon toxin produced by Clostridium perfringen bacteria type B crosses the blood brain barrier and binds to oligodendrocytes/myelin causing MS-like damage. One of several studies which support that position is an animal study:


                        Oh my goodness..I am on overload I will see my Dr at the RMmsC next month and will attempt to ask him questions re some of what you have presented.
                        Thank you for ALL your posts on this site !! You are SO informative !


                          I would think that if there was viral involvement we would see the virus reactivate when immune systems are tamped down with DMD. If not viruses "trigger" MS so we would have to vaccinate everyone against EB for prevention. With Tysabri being so specifically tailored to keeping the immune system out of the CNS and the results so effective for a med (68%), I imagine most of the research needs to stay focused on the autoimmune aspect of the disease.

                          I had sx since 1999 (hand tremors, altered judgement) and tested negative for CMV in 2013 for the purposes of choosing a negative sperm donor (which by the way lowers your applicant pool to 3% since it is about as common as chicken pox).


                            A successful treatment of SPMS without drugs was accomplished by Multiple Sclerosis Research Centre at the University of Queensland, Australia under the direction of Michael Pender. The treatment involved reducing Epstein-Barr Virus infected B cells. The patient’s name is Gary Allen, an interview with Allen can be found at:

                            MS is caused by EBV infected B cells accumulating in the brain because of poor clearance by cytotoxic T cells according to one theory. MS occurs as a result of impaired immune control of the Epstein-Barr virus in people who are pre-disposed to MS, according to that theory.

                            Gary Allen’s treatment yielded outstanding results. Research director Michael Pender described the process… “We collected about 400ml of blood from the patient. Then the blood is grown in the lab with an EBV vaccine for about 4 weeks. This retrains the T-cells (the cells which control the virus) and makes them more potent. Then we simply give the patient back the cells by injection into the vein about six weeks later.”

                            The idea is that the retrained T-cells go into the brain and kill the B-cells infected by EBV and by doing so hold back progression of MS and allow some recovery of function. For Gary Allen this treatment worked fabulously well.

                            You can read more about the research at:

                            If Pender’s theory is correct restricting B cells (EBV infected) from entering the brain (as Tysabri does) should slow MS. Tysabri is being trialed in progressive MS and may show effectiveness beyond RRMS if Pender’s theory about EBV infected B cells causing MS is right. Time will tell.

                            Also, it is reasonable to believe an anti-viral such as Raltegravir which is being used in the Charcot Project might diminish EBV infection of B cells and help curtail MS. Time will tell.

                            But the big news is that a treatment of SPMS using no drugs was highly successful.


                              This reminds me of Ann Boroch's story. In her book she explains about treating her MS in a similar way. It sure would be great if MSers could be treated effectively with anti-virals and anti-fungals. Good luck