Absence of Epstein-Barr virus in the brain and CSF

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Absence of Epstein-Barr virus in the brain and CSF

Post by MSUK »

Absence of Epstein-Barr virus in the brain and CSF of patients with multiple sclerosis - http://www.msrc.co.uk/index.cfm/fuseact ... pageid/707
MS-UK - http://www.ms-uk.org/
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Re: Absence of Epstein-Barr virus in the brain and CSF

Post by L »

squiffy2 wrote:Absence of Epstein-Barr virus in the brain and CSF of patients with multiple sclerosis - http://www.msrc.co.uk/index.cfm/fuseact ... pageid/707
Well, that changes things. And I had always thought the presence of EBV in us all explained the effectiveness of D3, HcCy and Rituximab.
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Post by gainsbourg »

Squiffy - did you miss the interesting EBV thread a couple of weeks ago? - 'Researchers find further evidence linking Epstein-Barr virus'

http://www.thisisms.com/ftopict-10536.html

The article you found was also mentioned by Dignan and I have repeated my reply below:
Actually, those findings don't surprise me because I believe the researchers are looking up the wrong tree. They are making the assumption that they need to find evidence of herpes attack .... but maybe there isn't any attack even though we know that herpes antibodies are produced in MS.

In war, an invading army doesn't necessarily need to fire a single shot in order to provoke a massive defensive bombardment - purely because it is considered to be a threat. That's what is maybe happening in MS, the presence of herpes hiding and cloaking itself deep in nerve tissue (in one shape or another) is enough to trigger a defensive response. This is mistaken as being the body attacking itself, in other words what seems to be an autoimmune response.

The Sargsyan study confirmed previous findings that herpes antibodies are there:

Quote:
"Anti-EBV antibodies were detected in the CSF of patients with MS"


This latest research ignores the fact that herpes antibodies are not found in the CSF of those without MS, or the fact that herpes antibodies (VZV at least) are known to increase in the CSF during MS attacks. Discoveries about herpes have been coming in thick and fast in the last few years. Locating it and understanding it seems to be as complicated as HIV. New discoveries are being made all the time - so don't rule it out just yet!
Coincidentally, there was another thread recently on TIMS ('Non MS Article') which was about how scientists now think that Alzheimer's plaques may be deliberately formed by the brain as a defense against invading bacteria and other microbes - even if these invaders are 'perceived' rather than actually active!

If something similar was causing MS plaques it would explain why they don't necessarily find evidence of active herpes attack.

For me the most likely explanation is that the mere presence (or hidden presence) of - EBV, VZV and other herpes viruses somehow acts as a threat or CATALYST and triggers what appears to be an autoimmune activity rather than because they are active.

If this is so, they can carry on searching as long as they want but they'll never find the evidence they're looking for because the viruses never need to be active, they never actually attack.


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Post by mose »

Let me start by saying I generally have only the slightest grasp on some of the things getting discussed here.

That being said, the presence of EBV antibodies in the CSF always interested me, but not from the angle I've seen it discussed. Wouldn't their presence in CSF just be another indication of what we've long known in that the blood-brain barrier is damaged in MS patients? Permeable blood-brain barier allows EBV antibodies, which are in almost everyone's blood, in. From my limited understanding, I wouldn't be shocked to see other unexpected, though normally occuring in the body, elements in CSF of MS patients.

To me, it does not appear to be the smoking gun some make it out to be. If I am off base, I would really appreciate being corrected.
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Post by BioDocFL »

I think what we will find is that many different pathogens can trigger an autoimmune reaction by affecting cells in a local environment, so we are not going to find one culprit virus that we can blame everything on. I believe that EBV just happens to be the most effective at it because it gets into B cells (and other cell types) easily and affects that host cell. Other cells that are drawn to the site can also become infected with EBV and perpetuate the local problem. Adenoviruses may be implicated in some cases of MS, not as often as EBV, probably because they are not as effective at invasion. Bacteria also could have an effect but to a lesser degree. I think it is all about cells being pirated and forced into generating autoantigens by the pathogen. Those autoantigens are probably of endogenous origin (i.e. abnormal proteins of the host cell) for the most part, not necessarily from the pathogen hidden in the host cell. I also believe that there may be cases of autoimmunity that arise without a pathogen due to a genetic flaw or some genetic or epigenetic damage from some exogenous material other than a pathogen (virus or bacteria).

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Post by rainer »

BioDocFL wrote:I think what we will find is that many different pathogens can trigger an autoimmune reaction by affecting cells in a local environment, so we are not going to find one culprit virus that we can blame everything on. I believe that EBV just happens to be the most effective at it because it gets into B cells (and other cell types) easily and affects that host cell.
I agree with this hypothesis and could see it as explaining the many of variations of "MS".

This line from the study throws me for a loop:
The frequency of detected intrathecal anti-EBV antibody synthesis in patients with MS did not differ from that in non-MS inflammatory CNS disease control patients.
The control group were patients with inflammatory CNS diseases? This seems incredibly stupid.
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Post by gainsbourg »

Mose - that is a good point about the BBB and it made me think, but on the other hand why do the VZV antibodies in the CSF skyrocket only during MS attacks?

Biodoc and Rainer - the many different pathogens (various micro organisms) hypothesis is appealing because that's what's known to precede Guillain Barre Syndrome and CIDP (the "autoimmune" demyelinating peripheral equivalents of MS).

Rather than having a single cause, MS is like an equation for which not even one of the missing components is yet known for sure. For me, the presence of herpes (EBV or VZV) is the closest we are yet to identifying part of the equation:

Herpes + (?) + (?) = MS

I think the other factors will turn out to be nerve nutrient deficiency (eg Vit B12, D3, zinc or magnesium) coinciding at the exact time of initial onset of MS.

I'm convinced the crucial mystery component (at that fateful time of initial pathogenesis) will turn out to be stress. Stress is known to precede MS attacks so frequently. Stress is known to procede herpes attacks....and nobody knows why on both counts. Stress is a trigger.

As I have said before, MS may be a disease where the brain damages itself! Stress laden thoughts somehow compromise or damage the very tissue from which they originate. Stress may somehow trigger a pointless defensive action against the threat of herpes attack.



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Post by gainsbourg »

I've dug up more about the coincidence of:

stress=MS attacks
stress=herpes attacks

Bear in mind that stress is the only factor known to frequently precede MS attacks.
Stress-related immune suppression: health implications (Glaser 1987)

This study used a year-long prospective design to assess linkages among distress, immunity, and illness. Serial blood samples were collected from 40 first-year medical students at the first, third, and fifth examination periods, as well as 1 month before each. There were significant decrements in the production of gamma-interferon by concanavalin A-stimulated lymphocytes obtained at the time of examinations. Antibody titers to Epstein-Barr virus (EBV) increased during examination periods, suggesting reactivation of latent EBV and therefore poorer cellular immune control of latent virus. We obtained data that suggest that T-cell killing by memory T lymphocytes of EBV transformed autologous B lymphocytes also declined during examination periods. The activity of a lymphokine, leukocyte migration inhibition factor, normally suppressed during recrudescence of herpes simplex virus type 2 infections, was altered during examination periods and an increase in both plasma and intracellular levels of cyclic AMP associated with examination stress was observed. An increase in the incidence of self-reported symptoms of infectious illness was also associated with examination periods. The data support the linkage between stress-related immunosuppression and health.

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