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Charcot Project, anti-viral trial

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  • Charcot Project, anti-viral trial

    The Charcot Project is a scientific study involving the human trial of a drug which blocks retroviral (HERV) replication. The drug involved is Isentress (raltegravir).

    There is evidence Isentress may also be active against herpes viruses such as EBV and HHV6 which have long been known to cause replication in HERV. The purpose of the Charcot Project is to determine whether an anti-viral medicine is effective in preventing progression of MS as tracked by monthly MRI.

    The ramifications of this trial cannot be overstated. Current MS therapies may be greatly altered or tossed aside if MS can be ameliorated using an anti-viral medicine. Research evidence continues to accumulate supporting the hypothesis that MS is an autoimmune reaction to latent HERVs within our genes which have become active.

    One of the most surprising findings of the Human Genome Project was the discovery that about 8% of our genetic material is viral. We now know that every person has HERV, literally in every cell. These residual scraps of ancient viruses embedded in our genes are called Human Endogenous Retrovirus, or HERV. Although residing dormant, HERV can be activated and begin to replicate, often as strings of proteins rather than as complete viruses.

    These strings of protein, HERV particles, are significantly overrepresented in Multiple Sclerosis brain tissue. People with MS have higher levels of HERV than those without MS.
    The HERV family includes MS-associated retrovirus (MSRV) which is very closely linked to MS prognosis and progression. Researchers have discovered that an envelope protein (ENV) of MSRV exerts a potent pro-inflammatory effect on immune cells and impedes myelin-making cells crucial for repairing the damaged protective sheath around axons.

    A monoclonal antibody (GNbAC1) to neutralize the ENV protein and permit re-myelination has been developed by a Swiss-based company, GeNeuro. Favorable early stage safety testing in people with MS was reported at a meeting of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) in Copenhagen. A subsequent report presented at a Boston MS Conference September 2014 revealed GNbAC1 decreased HERV-W Endogenous Retrovirus expression.

    In small human trials GNbAC1 appears to halt MS progression while removing the roadblock (ENV) which prevents re-myelination. GnbAC1 targets toxic ENV proteins but it does not induce immunosuppression; many current MS therapies suppress the immune system which creates opportunities for additional health problems.

    Large scale human trials will prove if GnbAC1 can consistently rescue myelin expression in MS patients.

    Halting disease progression and repairing myelin damage in people with MS would be the greatest advancement ever seen in the treatment of MS, IMO.

  • #2
    “There is now compelling evidence that EBV (Epstein - Barr virus) and HERVs (human endogenous retroviruses) are involved in Multiple Sclerosis”. “I think viruses are driving the disease.” Gavin Giovannoni, Chair of Neurology, London School of Medicine.


    • #3
      Thanks Apollo, makes more sense than a lot of the stuff out there. I have it on my radar now.


      • #4
        You are welcome, my friend. There are dozens of studies which give evidence that EBV is deeply involved in MS. Here is a recent one out just this month:

        Epstein Barr Virus Genetic Variants are Associated with Multiple Sclerosis.
        Neurology. 2015 Mar 4. pii: 10.1212/WNL.0000000000001420. [Epub ahead of print]

        “We analyzed the Epstein-Barr nuclear antigen 2 (EBNA2) gene, which contains the most variable region of the viral genome, in persons with multiple sclerosis (MS) and control subjects to verify whether virus genetic variants are involved in disease development.”

        “Our study unveils a strong association between Epstein-Barr virus genomic variants and MS, reinforcing the idea that Epstein-Barr virus contributes to disease development.”
        © 2015 American Academy of Neurology.


        • #5
          The Missing Link between EBV and MS appears to be that EBV activates HERV; HERV then provokes an immune response which becomes MS.

          Activation of MSRV-Type Endogenous Retroviruses during Infectious Mononucleosis and Epstein-Barr Virus Latency: The Missing Link with Multiple Sclerosis?

          “The etiology of multiple sclerosis (MS) is still unclear. The immuno-pathogenic phenomena leading to neurodegeneration are thought to be triggered by environmental (viral?) factors operating on predisposing genetic backgrounds.

          Among the proposed co-factors are the Epstein Barr virus (EBV), and the potentially neuropathogenic HERV-W/MSRV/Syncytin-1 endogenous retroviruses...

          During MS, there is no evidence of MS-specific EBV expression, while a continuous expression of HERV-Ws occurs, paralleling disease behavior.

          We found repeatedly extracellular HERV-W/MSRV and MSRV-specific mRNA sequences in MS patients (in blood, spinal fluid, and brain samples), and MRSV presence/load strikingly paralleled MS stages and active/remission phases.

          Aim of the study was to verify whether HERV-W might be activated in vivo, in hospitalized young adults with IM symptoms, that were analyzed with respect to expression of HERV-W/MSRV transcripts and proteins…

          …These novel findings suggest HERV-W/MSRV activation as the missing link between EBV and MS, and may open new avenues of intervention.”

          There may be triggers other than EBV which activate HERV but EBV is definitely one virus which does trigger HERV and appears to be able to activate HERV even during latency.

          Someone could test negative for EBV but it would not need to be an active infection which triggers HERV replication, it appears.


          • #6
            Those who want to know more about the Charcot Project may do so by viewing a fascinating introduction of it on YouTube at


            • #7
              More evidence that viruses contribute to MS and add to the possibility that MS may be treated with an anti-viral drug as a DMT someday.

              Remyelination impairment and HERV-W in Multiple Sclerosis

              Purpose : The human endogenous retrovirus type W (HERV-W) was shown to participate in autoimmunity and to contribute significantly to brain damage as it is observed in Multiple Sclerosis (MS).


              • #8
                The search for a viral cause in MS is active and worthy of our consideration to support, IMO.

                Quote... " Multiple sclerosis might not just be an autoimmune disease. Viruses could participate in causing the disease. Help us find out if we can treat multiple sclerosis with antiviral drugs.


                Why is this research hard to fund?

                Private sector funding bodies generally do not give finance to projects that use a generic drug… In addition, viral hypothesis regarding multiple sclerosis is an alternative direction of research, with the main working hypothesis being autoimmunity. As this is a slightly unconventional approach it is harder to gather the necessary support and funding." End Quote

                The link may be found via Google, "Help us find out if we can treat multiple sclerosis with antiviral drugs".

                Anyone not familiar with one of the most informative and popular MS blogs may want to check out:

                Or, just Google, "Why is EBV so important in MS"
                to find the blog.

                We can only find a cause and cure for MS if those looking are supported. I hope everyone will give thoughtful consideration to this present effort.