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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.
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.
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