Theoretical Immunology

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PointsNorth
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Re: A new concept and treatment options for MS

Post by PointsNorth »

Leo,

Maybe we use a dirt-cheap vitamin to do our dirty work?

Vitamin D: a link between Epstein–Barr virus and multiple sclerosis development?

http://informahealthcare.com/doi/pdf/10.1586/ern.11.97

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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

PN thank you for the paper on EBV and vitamin D. I think it is still a question whether vitamin D lies at the heart of a therapy or whether it is overhyped. The paper is from 2011. The direction in which I see things go and neurologists go would perhaps suggest more of the latter.
Last edited by Leonard on Thu Sep 18, 2014 4:30 am, edited 1 time in total.
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Re: A new concept and treatment options for MS

Post by Leonard »

Following my recent learnings, this is my best assessment of what is MS (update 18 September 2014).

The Human Endogenous Retro Virus (HERV) of the W-family is central to the development of MS as well as many other immune diseases. Herpes simplex, Varicella Zoster (VZV) and Epstein-Barr (EBV) are members of the family. During periods that people are immune compromised (can be the fetal period, the period of the newborn and immune deficient periods), the viruses can incorporate some of their genes in the DNA of permissible cells.

Immune deficient periods relate to the health of the intestine. Our diet (bad fats, gluten, low quality food) and our modern habitat (hygiene, lack of immune training) weaken the immune system. The immune system also weakens with age. A weakening immune system may initiate a vicious circle with poor gut health, enzyme and bacterial imbalances which will allow viruses and fungi to get out of control, and which affects later on the HPA axis lowering cortisol production in turn aggravating gut function. As such, the virus itself is not programmed to reactivate at specific time intervals but it is the immune system that weakens.

The gene transduction occurs during immune deficiency periods (this concerns newly infected cells, this does not refer to the 8% transgenic cells from the genome work). The incorporated viral genes (transgenes) are tolerant to the body or no immune memory against these transgenes has established. In MS, in particular the oligodendrocyte precursor cells (OPCs) will be infected. These oligodendrocytic stem cells and their progenitors are preferred by the virus because they differentiate and help replicate the virus. CCSVI is a factor that broke the BBB tissue much earlier.

People with transgenes in their body are healthy but predisposed to develop a disease. For instance, Crohn's disease is associated with measles. People predisposed to develop MS will become diseased when they are infected with a microbe that shares epitodes with the transgenes present in the OPCs. A chronic low-level EBV/VZV/Herpes infection/inflammation will cause such an immunological reaction. Vaccinations (e.g. Hepatitis) are also suspect.

Specific T- and B-cells will pass the CNS and cross-react with the transgenes in the OPCs (my count of EBV/Herpes B-cells is very high). Due to this cross-reaction, many OPCs will die which leads to a diminishing number of OPCs, of dendrocytes and a reduced myelination of neurons.

During this cross-reaction, many mediators will be released by the infiltrating T-cells. This will increase angiogenesis and cause hyperproliferation of surrounding tissue cells in the CNS which in turn causes the pathological lesions (sclerotic plaques) typical for MS.

The symptoms of MS will be mild in relapse-remitting MS but severe in progressive MS depending on the kind of virus that has incorporated part of its genome in the oligodendrocytic stem cells. Inflammatory viruses such as VZV will be associated with mild diseases whereas onco viruses such as EBV will be associated with severe diseases.


Personally I do not exclude the possibility that VZV prepares the path for EBV (microbleedings, angiopathy). And that the second peak in the age of onset is related to the EBV that starts to take its share.

I am very grateful to the eminent immunologist whom I consulted earlier this year for sharing this concept with me, the viral tolerance theory.

Besides the immune reaction against the OPCs, the high load of immune complexes has a second important effect. The lack of energy in MS and other lesions is a co-morbidity factor caused by the high immune complexes, the superoxide that reacts with nitric oxide and forms peroxinitrate, poisoning lipids, inhibiting ADP to ATP conversion (biochemical reaction hypothesis Scott/Pall). Hence, the fatigue typical for MS patients may be caused by the same chronic EBV infection but with a completely different underlying mechanism than the plaques in the brains. Because of high titers, I am eating my own muscles and with that also the connection between nerves and muscles; this is possibly an effect as important as the disconnect in the brains.

In my view, the main components of a therapy are to surpress the virus without reactivating it (e.g. by anti-HIV medication) and to resurrect the immune system (Pender, IgG3).

In the short term, a low-fat diet (Swank, low butyrate SCFA to stop EBV replication in the gut) and a 'vegetable' diet (Wahls flavonoids/Campbell fermented foods) will help strengthen the immune system (>90% of the immune system is in the gut). And possibly NMES to build muscle strength and muscle sensitivity.
Last edited by Leonard on Tue Sep 23, 2014 2:28 am, edited 1 time in total.
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

My right leg is weaker than my left leg, the right leg is thinner (circumference 2 cm less) and the muscles appear less developed.
Now, when applying electric stimulation, muscles in the left leg react faster, better, stronger than those in the right leg.

The signal that is applied via the skin will not travel through the brains back and forth, that is impossible (at best, there will be a bit of cross-talk in the local area).
It is locally applied and will work directly on the muscle.
Clearly, the sensitivity of the muscles in the left leg is higher than that of muscles in the right leg.

Therefore, I think that MS falls apart in a connection problem in the brains (due to demyelination) and a local problem of poor muscle sensitivity (and of course the problem with energy conversion - see above posting), all of them Herpes virus related.
Where the latter problem of low muscle sensitivity may in fact be as important as the former of brain demyelination.

[Afterthought: When it is cold outside, I go better and further. When it's hot, the contrary. This temperature dependancy is probably an issue of better/worse energy conversion and with that the feeding of mitochondria/ion pump determining muscle sensitivity. I think the temperature dependency demonstrates that not all of the neurological problem is located in the brains]

MS has remarkable commonalities with PHN (post herpetic neuralgia http://en.wikipedia.org/wiki/Postherpetic_neuralgia) including such things as muscle pain (nociceptors - the user manual of the NMES/TENS equipment I use Rehab X2 refers to the nociceptors) and muscle weakness (I think sensitivity is probably a better word). PHN is said to be the most common neurological complication of zoster (VZV) (above article Maria Nagel refers) where I would think MS is not very far apart.

Neuro Muscular Electric Stimulation (NMES) is said to be a promising treatment for PHN (both on the wiki page as well as in the article on VZV by Maria Nagel et al).
Likewise, NMES, as used by Terry Wahls, may be important to improve muscle sensitivity in MS.
And it is perhaps as important or more important than the diet.
Last edited by Leonard on Mon Oct 06, 2014 3:15 am, edited 6 times in total.
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MS made simple

Post by Leonard »

MS has multiple aetiologies.
All these factors are in some way combined leading to MS.
Ccsvi breaks the blood brain barrier
Environment (at youths vitamin D) determines cell structure
A period of immune deficiency allows viruses to anchor their genetic material in OPCs
An immune system that produces high concentration of useless B-cells/immune complexes that attack own tissue
And, possibly, a late maturation of the kidney/renal system

MS falls apart in several main problems.
And again, all these factors are in some way convolved in patients with MS.
'Auto'- immune reaction by immune complexes causes sclerotic plaques and demyelination
Virus causes (post) herpetic neuralgia (weakening of nerves / muscles)
Biochemical reaction NO OHNOO inhibiting ADP to ATP conversion weakening energy and cellular nutrition
Bacteria (Lyme, Cpn ..) get their chance when weakened immune system causing other problems

New MS treatment paradigm
New anti-viral therapies are very promising

We must find ways to find support for this concept.
If any one has ideas, please let me know.
Last edited by Leonard on Thu Oct 09, 2014 1:27 am, edited 3 times in total.
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

http://owndoc.com/lyme/multiple-scleros ... -cover-up/

I do not agree with the title of this article or its contention. I do not believe that MS is caused by bacteria. I think that the herpes family of viruses stands at the basis of MS. When the immune system weakens because it is fighting the virus, bacteria get their chance including Borrelia and Cpn.

But besides that, the article is not without its merits when it examines the reality on the ground. If you read the article the smell is definitely there that MS Societies, big pharma, patient advocacy groups and MS experts are all elements of a bigger MS eco-system that is completely locked-up. Stagnant.

In this context, it is noteworthy that the MS Associations have formed the MS Progressive Alliance to study what exactly is and is causing progressive MS. Now, only now, anno 2014, 175 years after Charcot, decades after new theories on MS were developed.

I find this rather late in the day. Are they afraid that one day they will be overtaken by events? Overtaken by ideas on patient fora such as this?

Of course they knew each other before; and of course they must have met at various occasions, year after year. Remarkable that now suddenly they know how to find each other, on progressive MS. Did it never cross their minds before to take such an initiative - the silence? Or did it?

Let us hope that now that the viral dimension is out as it was clearly mentioned in the opening speech of ACTRIMS/ECTRIMS 2014 by Hafler, the sector will take its responsibility, a big responsibility. There are millions of people with MS waiting. If the sector would accept the ideas behind this thread, I am sure we could make rapid progress with devising effective therapies for MS.
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

The immune system weakens for a variety of reasons. The health of the gut microbiome certainly reflects or correlates with immune system health.

When the immune system runs down, the herpes family of viruses resurfaces. It is never away, it is latent and kept under control by a healthy immune system. When the herpes virus resurfaces, the immune system "gets occupied" with the virus, produces relentlessly non-working immune complexes, and "forgets" about fungi and bacteria which then get their chance.

The virus is with us for a lomg time, in our own life but also with us as human beings. In periods of immune deficiency, it anchors its genetic material in permissible cells, including for instance OPCs, without immune memory being established.

If later on a virus resurfaces that shares common epitodes, the immune complexes start circulating and cross-react with transgenic cells that were infected before. This explains auto-immunity and the formation of the typical MS plaques in the brains.

But the virus does other things too. The immune complexes, through a biochemical reaction, cause a high level of peroxynitrite. This causes huge oxidative stress, jams the cells and inhibits the ADP to ATP conversion. And it poisons fat tissue and causes lesion in the brains. I think it also causes what is called herpetic neuralgia where fibromyalgia is not far away.

MS is thus a convolved issue of connection problems in the brains (demyelination) and connection problems in the periphery with the muscles/nerves as well as mitochondrial failure and fatigue resulting from poor cellular feeding and function.
Last edited by Leonard on Sun Oct 19, 2014 2:32 am, edited 2 times in total.
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Re: A new concept and treatment options for MS

Post by kengriff »

Anti-virus therapies are most commonly used for various types of diseases associated with viruses. These technique is much more beneficial than any other treatments. I also think that it would be more promising for the treatment of MS.
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Scott1
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Re: A new concept and treatment options for MS

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Hi Leonard,

My own recent experience makes me firmly believe that the Th1 activated response is an inflammatory reaction to bacteria and is separate (but maybe connected) to the EBV/ peroxynitrite mediated pathway. My recent, severe attack occurred after I started taking n-acetyl-glucosomine. I freely admit I failed to do my homework properly. My suspicion is the damaging demylination occurs when Th1 recruits CD4 and then CD8 gets involved so we need to shift Th1 to Th2. (That's the reason I now take dimethyl fumurate but I can only hope that time helps me remylinate not the drug.) The NAG is a key ingredient in hyaluronic acid which can be seen in the myelin plaques but it also is key to peptidoglycans which are the cell walls of gram positive bacteria. The peptidoglycans (or even fragments of them) provoke Th1 and a cascade begins. This is a separate mechanism to the peroxynitrite.
It would seem to me that the leaky gut is the pathway for pathogens to gain entry to inappropriate parts of the body. The leaky gut would relate to a shortage of vitamin A and retinoids because megalin as a transport agent is failing in the renal system. This failing would be confirmed by other vitamins (D and B12) being affected at some point. It doesn't have to be forever. Just long enough for the pathogen to gain entry. As a precaution I now take Zinnat as a long term antibiotic as it can dismantle peptidoglycans. We would need to do this to remove an agent for inflammation. Perhaps (who knows) the variability of progression depends on the quantum and species of bacteria and it is the cell wall that is the trigger.
EBV seems to me to be all about fatigue (disabling glyceralderhyde-3-phospate), the peroxidisation of lipids and the other disturbances and is crucial to progression of MS but not necessarily major demyelination. The interesting thing I noticed in my pronounced demylination was the complete absence of fatigue. I assume that's because I was back on valacyclovir to limit superoxide overproduction and was still taking 750 mg a night of coenzyeme Q10 which substituted for glyceraldehyde-3-phosphate so my cells were able to respire properly. I know I have the team in this hospital stuffed because my only MS symptom is demylination. They keep wanting to know if I'm fatigued but I'm not at all. I've been tripped up by peptidoglycans but I'm sure we need to separate the disease and its progression differently than is done now.
I would say;
Step 1 Neonate or first 2 years of life there's a renal problem
- results in production of ADMA which leads to issues including too much iNOS, impaired processing of Vitamin A, B12 and D and problems with vasodilation
Step 2 Step 1 problems weaken the system
- in particular the gut does not seal properly and pathogens of any type can gain an inappropriate entry
Step 3 a viral infection
- most likely herpes family which take up permanent residence in the host cells (in particular EBV)
Step 4 Infected host cells produce excess superoxide which combines iNOS mediated nitric oxide to produce peroxynitrite
Step 5 somewhere in the preceding steps MS myelin ceases to harden and remains soft like an infant up to the age of 6 and prone to demyelination
Step 5(a) Peroxynitrite levels build over time inducing fatigue, lipid problems (LDL etc) and on and on
Step 6 something triggers a Th1 inflammatory response to bacterial cell walls which exaggerates demyelination.
The problem will be identifying bacteria because they wont find just one and the location and infection levels will vary in each case.
The only "autoimmune" part of this is the cycle of Th1 activation. My feeling is the longer I put up with this the more involved my lymphatic system became. As it kept flooding me with lymph that made me feel as though there was too much pressure under the skin. In much the same way that an ingrown toenail gets worse and worse as inflammation creates pressure that signals a stronger immune response. The greatest points of discomfort on me could be mapped on a diagram of my lymph node pattern. The pressure from Lymph provokes Th1 to keep recruiting CD4.

So it's multilayered but not all layers obviously link to each other. This description wouldn't be the end of it just a skeleton for the flesh to hang on.

Regards
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

Scott,

sorry to hear about your relapse.

The immune system is tremendously complex where the implications of oxidative stress are perhaps not fully understood.
The NF-KB is certainly involved that controls in some way the immune response and Th actions.
I just read in the book "Explaining unexplained illnesses" from Martin Pall about his views on possible mechanisms.

I don't feel qualified to assess the steps in your theory.
What this needs is qualified people that knock their heads together.
Besides neurologists and immunologists, biochemists and virologists should be involved.

Leo
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

Let's park the connection problem in the brains for a moment and focus on the peripheral neuropathy.
http://en.wikipedia.org/wiki/Neuropathy
http://en.wikipedia.org/wiki/Monoclonal ... gnificance

I see here a very large number of overlapping diseases with different names. Peripheral neuropathy, (post) herpetic neuralgia (PHN), fibromyalgia (in remote), mononeuritis multiplex, poly neuropathy, monoclonal gammapathy of undisclosed significance, disease of gamma globulins, mitochondrial energy failure, lupus, …

And I see signs and symptoms that we recognise: slowly progressive symmetric distal sensor motor neuropathy, muscle loss (my blood test showed two deficiencies: the high load of herpes immune complexes and high titres showing muscle loss), urine retention, pain worse at night, fatigue, Ca levels and inactivate pump mechanisms (see pg 13 book Pall below) etc.

And common underlying infections: herpes simplex, Varicella Zoster, bacteria, Hepatitis-C etc. etc.

In our current system for medicare, every expression of a neurological set of symptoms got its own name, based on several types of observations. But in fact, a bigger common scheme may be underlying. A scheme that encompasses the wide variety of observations, their patterns of case initiation, their chronic nature and many of their shared and unique symptoms and signs of the chronic phase of the disease. A scheme that explains many unexplained observations by a simple conceptual framework.

I believe that all these diseases may be explained by a combination of biochemistry and (Herpes) virology. As Martin Pall titles it in his book "Explaining unexplained illnesses": A Major New Paradigm of Human Disease. And I believe that MS finds an explanation here too.
Last edited by Leonard on Fri Oct 17, 2014 6:50 am, edited 1 time in total.
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Re: A new concept and treatment options for MS

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Hi Leonard,

I do agree it's multifactorial. The question will be "why us and not others?" A lot of research shows things like shifts in magnesium and zinc, elevated iNOS, low vitamin D, low uric acid and so on as well as demyelination. Unfortunately they like to lump things together as MS and chase magic bullets. I'd rather they say it might be a bunch of infections on top of a metabolic base.
Now in the press they are chasing single cell organisms. Still trying to find one guilty party.
I do think solving what is metabolic will be critical to blocking the infections that lead to disease progression but they are a long way from that at the moment. Other people have the infections (EBV etc) but don't get sick. We do.
That's why I think something is wrong in early development that leaves us vulnerable.

Regards
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Leonard
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Re: A new concept and treatment options for MS

Post by Leonard »

Scott,

Thank you for these observations.

I think that CCSVI is a factor that makes us vulnerable. The vein truncation is most likely a birth defect. A thickening of veins may be caused by viral expression. Then CCSVI may be caused by a combination of factors.

With CCSVI, the blood flow gets impaired. And eventually, the very thin tissue of the BBB breaks. This leaves our OPCs vulnerable for infection by virus.

I think it also causes other things such as an obstruction of the normal flow of Cerebral Spinal Fluids. The CSFs drain in the IJVs. This in turn causes all sort of problems for the grey matter.

My son is doing well in life. But in times of stress - I see this high workload related, an EBV infection re-emerges (because his immune system runs down). Incidenty, this seems to occur typically in late Spring, when immunity is low. Is the virus already settling itself here in permissible cells without immune memory established to cause auto-immunity later in life?

Now he won't get MS later in life because he does not have CCSVI. He and my eldest daughter were tested on CCVSI by echo-Doppler by a very experienced interventional radiologist who must have seen over a thousand MS patients. Their IJV's were o.k., no signs whatsoever of narrowing, when pressed by the pod a perfectly normal response. Still, the EBV infection may cause other problems later in life such as diabetes 2, coronary artery aneurism, etc etc. A golden question is: should he use Zovirax of valacyclovir early in life to get the virus down?

Having said this, I think CCVSI is most definitely a factor. I was diagnosed with CCSVI Pattern C in 2009 by Zamboni himself. A truncation as in the textbooks in the right IJV, probably a birth defect; a dominant left IJV must have developed for that reason. An obstruction behind the left ear, may have come later in life and be virus related. I saw the comfort with which he assessed my situation by the echo-Doppler. This was not black magic, this was real science. My IJV's were almost entirely blocked; the Azygos for 50%. Since then, they have been opened but clearly the BBB had already broken at 14 years of age when I had my firt symptoms (loss of control of left hand).

Now obviously, MS is more complicated than CCVSI. The virus is causal. I very much agree with the words in your last posting except for this one: "I do think solving what is metabolic will be critical to blocking the infections that lead to disease progression…"

I do not believe that our problem will be solved by metabolic factors. For sure, hormones are an influence. Hormonal deficiencies often relate to symptoms belonging to CFS or fibromyalgia or other auto immune diseases. The HPA axis may be affected at some point causing further hormonal deficiencies. And by administrating hormones, you may correct certian things and in fact help the immune system a bit.

However I think while treatment with hormones may help, it is not enough, is not convincing. It is the virus that needs to be tackled, by the immune system or by anti-viral medication. Without tackling the virus, the problem will persist.

Leo
Last edited by Leonard on Sat Oct 18, 2014 11:55 pm, edited 2 times in total.
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Re: A new concept and treatment options for MS

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Hi Leo,

That's the point I'm trying to make. Once infected you do have to tackle the virus but before you have a virus what is going on? Is it the status before a viral infection that makes a difference?
I have a very good friend who has had glandular fever as a child, as I did, but she is unaffected. What is the difference between our paths. Did I have a different strain or did she get infected when her metabolic health was better than mine? Or was it both things.
Is it the virus or the product of its infection that is the problem? My view is it is peroxynitrite as there is plenty of evidence it is a disabling radical. To make peroxynitrite you need superoxide (EBV infected B cells) and Nitric Oxide. The Nitric Oxide relies on nitric oxide synthase. The constitutive forms (endothelial and neuronal) are fine but why do we have high levels of the inducible form which is made in response to injury? Are we injured already or is the body fooled into thinking it is injured? If it is not injured but behaves as though it is then that would seem to me to be metabolic. If it not metabolic malfunction then we need another reason to make an abundance of iNOS. We also need to say what limits the constitutive forms of NOS so iNOS becomes the natural state.
Do healthy people who control their prior infection make as much superoxide from EBV infected B cells as we do? I presume molecule vs molecule they probably do. If peroxynitrite is the dangerous product then where is theirs? If they don't have as much then what controls their iNOS. That's the bit I think is metabolic in the puzzle.
Absolutely control the virus when you have it. It's life before the virus that intrigues me.

Regards
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Re: A new concept and treatment options for MS

Post by Leonard »

Hi Scott,

According to Martin Pall in his book "Explaining unexplained illness" (see link below), short term stressors that initiate cases of multisystem illnesses act by stimulating nitric oxide synthase (NOS) activity and consequently produce increased levels of nitric oxide and its oxidant product peroxynitrite. Initiation is converted into a chronic illness through the activation of vicious cycle mechanisms through which chronic elevation of nitric oxide and peroxynitrite is produced and maintained.
All three nitric oxide synthases have been shown to be involved (eNOS, nNOS and iNOS).
An increased NF-KB activity will lead to increased iNOS activity by stimulating through the inflammatory cytokines IL's, TFN and IFN the activity of the iNOS gene itself.
There is a combination of stability and instability, positive and negative feed back loops, leading to what is essentially inflammatory biochemistry, he describes in his book.
For sure the peroxynitrite is pretty bad, triggers oxidative stress, immune response, effects on the mitochondrial electron transport chain, pump inactivation, depletes energy in the form of ATP etc.

http://www.amazon.com/Explaining-Unexpl ... 078902389X

You mentioned earlier that EBV immune complexes release superoxide. Superoxide is a parameter too in the model by Pall. Do you have any good references for - if I remember well - the two molecules of superoxide released by the immune complexes? Could this be a factor that helps trigger the disease?
Pall mentions viral infection as a short term stressor, and he mentions phagocytes as one of many elements that produce a respiratory burst that uses a large amount of oxygen to generate superoxide.
Considering the chronic nature of immune complexes in our case, this mechanism might well become a key trigger of the vicious cycle, in particular if we assume a viral causation for MS.

Leo
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