I have written quite a bit about the connection between wayward expression of an ERV, and Multiple Sclerosis.
I am very comfortable saying there is a connection between ERV expression and MS. I am not confident in saying 'If we destroy the cells producing this ERV, we will stop MS.'
I totally get that the ERV protein in question, an Env, can be inflammatory in the brain, so knocking that out might stop some inflammation/damage in the brain.
But the cells producing this ERV are not tumors. They are not virally infected cells. If this Env is being expressed because of epigenetic modifications, then targeting the Env cells will not necessarily help. I would think you need to target the environment allowing the development of these cells. If you dont, it seems like all you will do is, for example, kill 5 Env expressing cells, and then 5 more will take its place, over and over. Having a lot of cell death (even controlled, purposeful cell death) going on can be bad for the patient.
Buuuut it seems some people are willing to try an anti-ERV therapy in the form of a therapeutic monoclonal antibody, GNbAC1, in the hopes it will stop MS. Because the ERV they are targeting is not a 'retrovirus' that changes all the time, but a 'retrovirus' that has become a part of us, they can fairly confidently create antibodies that will target the ERV Env protein on the surface of cells. Once this antibody binds to the target cells, the antibodies can either directly lead to death of the cell, or they can recruit effector cells that will kill the Env expressing cell.
They have given various doses of this therapeutic anti-ERV antibody to healthy patients (Phase I clinical trials) and nothing obviously 'bad' happened. And, now they have given the anti-Env antibody in various doses to MS patients, and nothing obviously 'bad' happened (Phase IIa).
The next goal will be to see what kinds of doses they have to give MS patients to see any positive effects (if any dose will lead to positive effects), and then see if anything 'bad' happens at those doses.
I really hope this works out, for the researchers and the patients! I just dont have those hopes up too high. Im not sure if this is the best idea...
Seems like this is shutting the barn door after the horse has left, or whatever that saying is. The inflammation leading to MS seems like a plausible etiology, but once the T-cells get going and you actually have symptoms, the cascade seems like it would be hard to stop.
Maybe this in combination with Natilizumab, so you stop the T-cells from getting in, and then block the inflammation so they don't come back?
I dunno about any of this, but here's the latest thing I've read about possible new developments in MS.
'Toxin-Emitting Bacteria May Be Environmental Trigger for MS'
Already researched in Denmark 350 RRMS patients and SPMS patients have the Herv FC1 virus another study reveals PPMS patients have the Herv fc 16 virus