I think your understanding of studies that remnants of the Epstein Barr Virus (among others) imbedded themselves in human genes over millions of years of evolution is correct. A retired immunologist recently explained me exactly the same.
I find this information from the above mentioned thread most interesting: The sequencing of the human genome revealed human endogenous retroviruses (HERV) represent more than 8% of the human genome and result from the integration of exogenous retroviruses DNA during the primate evolution.
The information on this same posting from Fred1208 carries on by saying: MSRV is normally latent in the genome of individuals, but it can be re-activated by certain co-factors to expresses a pathogenic protein, MSRV-Env. Recent evidence has demonstrated that this ENV-protein is expressed in MS lesions from an early stage, is pro-inflammatory and inhibits remyelination.
The study that I quoted in my posting of March 12, here above, is precisely on this point. I will post it here again for ease of reference: http://www.ncbi.nlm.nih.gov/pubmed/23836485 And indeed, I found the study on the GeNeuro website.
@leonardo: I think EBV itself is the issue. Its envelop protein inhibits OPC differentiation and therefore should be earmarked as the direct cause of MS/demyelination. It could even be that the cross-reaction of immune complexes with the shared epitodes of remnants (what we know as autoimmunity or the action against the 'self') and the interaction with the fat metabolism (now subject to a lot of study e.g. from Buffalo) are secondary.
The fact that the EBV is on the OPCs is not a big surprise as such. The virus has learned to get on to stem cells because in that way replication becomes much easier.
Now on the question why the EBV can emerge as a chronic active disease, indeed a weakened immune system is the cause for not controlling EBV. And as you say, problems with the B-cells and T-cells come around the corner here. Again, EBV may play a double role here if it infects the stem cells of the bone marrow. And as we saw it has preference for stem cells. But also our diet, anti-oxidants etc are influences. It is a multi-facetted issue.
I think the CSF study you refer to also applies to MS and probably to a whole lot more. The site of GeNeuro is quite instructive.
Anonymoose wrote:Hi Leonard & all,
I just find myself unable to apply further thought to the ebv/ms issue. As of now, there is no proof that ebv is running some of the ms shows. We don't know all that it does or how it works. Seems a fruitless labor for a lay person to try to figure out how it makes things go awry in some. The only thing that can be done is experimentation. So, I'm experimenting. It will be decades before they tie down all the ways in which ebv effects us. I'll just be happy with improvements/stability if any is to be had from an ebv killing crusade.
thank you. I am not sure whether it will be decades before they tie down, we live on Internet time. But just like you, I would be happy with improvements/stability if any is to be had from my Zovirax ebv killing campaign. The hope is that the chronic EBV disease will be pushed down and that then the immune system (that may also be EBV infected itself as well as the B-cells it produces) will regain strength to take over and keep the thing down.
I will let you know if there is anything to report but be prepared for a slow process, just as it came…