grandsons4 wrote:CaliReader, thanks. The article reinforces, in part, my thinking as concerns the EBV/MS connection, but also raises new questions. The researchers looked for antibodies. Is it possible to carry the EB virus and not develop antibodies? If so, could whatever triggers MS simultaneously trigger a fight against EBV? As for now, I'll keep researching and recommending to my son to treat with an emphasis on mitigating effects of EBV.
I love that article. It's been quite a while since I've posted anything but this conversation has got me interested.
When I first started trying to sort myself out I noticed the large body of work that associated EBV with MS. Later I became aware of the work that looked at Peroxynitrite as a rather pernicious problem.
My approach to the EBV was to take 2x 500mg of Valacyclovir twice a day (see Avonex and Valtrex in the regimes forum). I did this for over 10 years and, for me, it was very successful. I can understand the problems you have had taking it but I suspect your adverse reaction is due to how the Valtrex is reacting with other aspects of your general health rather than the EBV. You may need to ask the question-"what other bugs do I have as well?" You are on the right track but the path is often not clear.
The reason you should still aim to attack the EBV is mentioned in the article. The EBV infected B cells are immortalised by EBV and that is not good. Those cells give off an excess of Superoxide. In itself that's a radical but not the end of the world. The problem arises when Superoxide meets Nitric Oxide. There are two forms of Nitric Oxide- 1) Constitutive (good) and Inducible (Bad). Constitutive has two forms- 1) Neuronal and 2) Endothelial. Inducible Nitric Oxide arises in the absence of Constitutive Nitric Oxide. It is common at the sight of wounds and has a longer life than constitutive Nitric Oxide. If Superoxide meets Inducible Nitric Oxide there is a exponential expansion of the product Peroxynitrite.
Peroxynitrite does a lot of rotten things but the worst is it knocks out Glyceraldehyde-3-phosphate, a central step in glycolysis and gluconeogenesis. This means you are short of phosphate required for ATP to drive the sodium -potassium pump in all your cells to create energy. Signs that this is happening are very low levels of non essential amino acids, low uric acid, elevated LDL levels etc.
I took so much Valtrex that I ended up with gout (because it's a purine). I was forced to relook at everything I did and eventually will get around to posting a long article.
In essence, to stay well, this is what I do now.
1x 300mg Resveratol on rising
1x large glass of pomegranate juice
2x really good probiotic tablets - or you will have a problem
A bowl of greek style natural yoghurt
3 boiled eggs
After half an hour
1 large freshly made carrot juice with a big chunk of fresh ginger
A level teaspoon of L-Arginine powder in a glass of water- (tastes disgusting but this is critical)
450-600mg of Coenzyeme Q10 just before going to bed. (also critical)
I am amazingly well and rarely think of MS any more.
If I was you I would establish a base line using a Fasting Amino Acid test to see if your nonessential amino acids are low. I bet they are through the floor.
low uric acid is directly correlated with zinc status, an essential nutrient which is known to be low in ms patients and is critical to a wide variety of body processesThe low uric acid arises from the disruption to the glycogenic cycle. In particular the way the Krebs cycle is affected.
Perron has founded a biotech start-up —GeNeuro, in Geneva, Switzerland—to develop treatments targeting HERV-W. The company has created an antibody that neutralizes a primary viral protein, and it works in lab mice with MS. “We have terrific effects,” Perron says. “In animals that have demyelinating brain lesions induced by these HERV envelope proteins, we see a dramatic stop to this process when we inject this antibody.” He is scheduled to begin a Phase 1 clinical trial in people with MS near the end of this year. A clinical trial with schizophrenics might follow in 2011.
Vascular endothelial cells are suspected of being the target of autoimmune processes seen in many connective tissue diseases and in systemic vasculitis as evidenced by the detection of circulating autoantibodies against endothelial cell antigens. In order to select B cells recognizing endothelial cells antigens, Epstein-Barr virus (EBV)-infected B cells, obtained from one patient presenting a systemic vasculitis, were cocultured with human endothelial cells concurrently with a human endothelial cell line (EC-pSV1 cells). This coculture consisted of a first step of expansion of B cells specifically selected by adherence onto human umbilical vein endothelial cells (HUVEC). The adherence of selected B cells was specific to endothelial cells because no rosette formation around control cells (HeLa cells or COS cells) was observed. Adherent B cells were cloned by limiting dilution by coculture onto EC-pSV1 cells and screened for anti-HUVEC antibody production by endothelial cell ELISA. An increase in anti-HUVEC antibody production of IgM isotype was detected by endothelial cell ELISA, peaking at Day 9 and remaining constantly elevated, relative to B cell expansion. Among 21 B cell lines producing IgM, 6 presented high levels of anti-HUVEC antibodies, whereas 1 of 52 B cells cloned without EC-pSV1 cells showed such antibody production. Anti-HUVEC antibody production and B cell proliferation were dependent on the presence of endothelial cells. Two of these 6 B cell lines produced antibodies directed against an endothelial cell antigen with an apparent molecular weight of 192 kDa as determined by immunoblotting analysis. Our results demonstrate that adherence of EBV-infected B cells to endothelial cells and further cloning by adherence can efficiently select anti-HUVEC antibody-producing human B cells and might help to define antigens potentially involved in autoimmune diseases.
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