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Epstein-Barr virus disrupts blood-brain barrier, predisposing to MS



Epstein-Barr virus infection of human brain microvessel endothelial cells: A novel role in multiple sclerosis

Abstract
Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. ... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... pageid/707

Have the full paper and have been very interested to read it this week...specifically looking at the interaction between a weakened BBB and venous reflux. If it were merely a matter of EBV weakening the BBB, lesions would be found throughout the MS brain, but they are not. They are venocentric. Believe this may very well be another part of the puzzle--
thanks for posting,
cheer

The more I hear the more I am convinced that herpes plays a role in MS. Why do I think this?

1. Herpes lives in nerve tissue - MS is a disease of damaged nerve tissue.

2. MS is virtually unknown in people who have never had the Epstein Barr virus.

3. An experiment a year or so ago revealed that herpes DNA (Varicalla, i.e. chicken pox) was found in the spinal fluid of all those tested who had MS (increasing 500 fold during attacks) but not in any of the controls.

4. MS attacks very often occur following mental or physical stress - so do herpes attacks.

5. If MS is triggered by herpes, it may explain why venom from bees, snakes, scorpions and jellyfish sometimes relieve MS symptoms .....perhaps the venom is simply killing the herpes! Apparently cobra venom is the only substance in the world known to kill herpes.

6. Sardinia and Sicilly have two of the highest concentrations of MS in the world (despite all the sunshine) - but they have the highest incidences of Herpes Virus -6 related cancer.

7. And now we learn that EBV disrupts the BBB.

Okay, I know that evidence of herpes actually attacking nerve tissue has never been shown but maybe it doesn't have to actually attack. My guess is the mere presence of herpes somehow stimulates (or scares) the immune system into periodically attacking the tissue where the virus resides.



gainsbourg

J Neuroimmunol. 2011 Jan;230(1-2):173-7. Epub 2010 Sep 9.
Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis.
Casiraghi C, Dorovini-Zis K, Horwitz MS.

Department of Microbiology and Immunology, The University of British Columbia, Vancouver, British Columbia, Canada.
Abstract
Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis.

Copyright © 2010 Elsevier B.V. All rights reserved.

I don't think an active inflammation is necessary, because EBV still produces proteins when it is inactive.

Super exciting stuff. Folks may try to ignore it, but it makes great sense.

It has also been proven that people with MS have immune systems that overreact to EBV. It doesn't need to be an acute onset of mono to be responsible for MS, just a little flare up here and there will do.

I believe that at a young age when the thymus is producing naive white blood cells, paired with a horrible diet and low vitamin D, there is a situation where the fat that makes the blood brain barrier (BBB) is brittle and contains many of the precursors of bad-prostaglandins. When the BBB is assaulted by any foreign element, especially a retrovirus like Epstein Barr, it over reacts. (Epstein Barr is incredibly interesting in its effects on the BBB and vasodilation as it travels back and forth across the BBB). This causes a cascade of inflammation which signals white blood cells to arrive. Since these are naive white blood cells, they are still becoming sensitized to foreign elements. Once they pass the BBB to fight off the foreign invader, they tend to stay busy if they cant find any thing else to fight. Well, they are not supposed to be in the CNS and can't get out as easy as they came, so the myelin sheath seems more and more foreign looking and they begin treating it like a virus and going to work. Then they become sensitized to the CNS myelin. Congratulations, ten years down the road you have MS. I guess the best bet is keeping the little buggers out of the CNS.

Posted this out of place in CCSVI board. It fits here better.

So how do we get rid of epstein barr or at least take something to inactivate it.
Any ideas?

MSBOB wrote:J Neuroimmunol. 2011 Jan;230(1-2):173-7. Epub 2010 Sep 9.
Epstein-Barr virus infection of human brain microvessel endothelial cells: a novel role in multiple sclerosis.
Casiraghi C, Dorovini-Zis K, Horwitz MS.

Department of Microbiology and Immunology, The University of British Columbia, Vancouver, British Columbia, Canada.
Abstract
Multiple sclerosis (MS) is an inflammatory neurological disease that is widely regarded as the outcome of complex interactions between a genetic predisposition and an environmental trigger. Epstein-Barr virus (EBV) has recently been associated with the onset of MS, yet understanding how it elicits autoimmunity remains elusive. Neuroinflammation, including the entry of autoreactive T cells, likely follows a breach of the blood-brain barrier (BBB) leading to CNS lesions in MS. We show that EBV can infect human BBB cells leading to increased production of pro-inflammatory mediators that result in immune cell adherence thus modeling a key step in MS pathogenesis.

Copyright © 2010 Elsevier B.V. All rights reserved.

On this thread http://www.thisisms.com/ftopict-15188.html it was suggested that the stenoses cause Nitrogen Oxyde NO2. Normally this NO2 is to relax the vessel walls. But for the stenoses that won't work. Because of sustained narrowings and high NO2 levels, the NO2 will leak slowly through the vessel walls and inflammate the myeline. Apparently, from what I understood from a posting, the NO2 needs a virus to trigger the process. So is EBV the trigger where the narrowings prepare the environment?

I also read recently that DMDs have an anti-viral mechanism to them. Though I am unsure of the source. Could have been on this forum though.

Also - not all MS lesions are venocentric. I believe Pattern III and IV lesions are not venocentric, but I could be wrong. Here is the paper on Lesion types. http://www.direct-ms.org/pdf/Immunology ... ypesMS.pdf

LR1234 wrote:So how do we get rid of epstein barr or at least take something to inactivate it.
Any ideas?

A high lysine to arginine ratio is reputed to help fight herpes.

Answer therefore Lysine supplements.

Edit - chicken and beef protein are high in lysine. Also pulses and fish

zinc deficiency is common in ms, and impairs the integrity of the blood brain barrier.

zinc is anti-viral. so is selenium (another one that is low in ms patients).

the recommended daily amounts are already in the best bet supplement recommendations:
•Zinc: 25-50 mg
•Selenium: 200 mcg (you can get it from 2 brazil nuts)

hope that helps

i saw a web site recommending the antioxidants a c and e also. also mentioned b complex, and magnesium. so basically everything. may as well throw in the vit d3 for good measure.

I had EBV in college. I am a chronic carrier. I was exposed to two students at the college where I teach with active EBV and my titer shot up to 3 times normal. My neuro prescribed Acyclovir 800 mg 2 X day.