This Is MS Multiple Sclerosis Community: Knowledge & Support

Might some forms of neurological illness, such as multiple sclerosis and schizophrenia, be caused at least partly by bacteria, viruses or other parasites? A largely Danish team has recently published evidence of a strong association between multiple sclerosis and a retrovirus, together with hints that a gene called TRIM5, which is used by cells to fight viruses, is especially active in people with MS.

Other illnesses have unexpectedly turned out to be caused by parasites. In the 1980s, Barry Marshall of the University of Western Australia ran into a brick wall of official disbelief for suggesting that a bacterium caused stomach ulcers. Only by deliberately infecting and then curing himself did he finally get the medical establishment's attention (and eventually the Nobel Prize).

The virus implicated in multiple sclerosis is called HERV-Fc1, a bizarre beast called an "endogenous" retrovirus. What this means is that its genes are part of the human genome. For millions of years, they have been integrated into our own DNA and passed on by normal heredity. It was one of the shocks of genomic science to find that the human genome contains more retroviral than "human" genes: some 5% to 8% of the entire genome.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/3392

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i some pwMS had mononucleosis earlier in life

So far I count a handful of viruses and a similar amount of bacteria that are thought of being the cause and/or contributing to MS. How can all these studies have essentially conflicting conclusions? HERV, EBV, HV6, Cpn, etc. I guess it just doesn't make sense that all of these could the culprit. Strange.

What Dr. Wheldon wrote regarding endogenous retroviruses:

Endogenous retroviruses have been suggested as participants in the progression of MS. These ancient sequences of virus DNA are replicas of those inserted into the genome by an accident of infection during germ-cell formation.

Might HERVs play a role in the development of MS? It seems possible. Activation of the HERVs HERV-H/RGH, HERV-W and ERV-9 was described when specific cell types (mainly B cells) from MS patients were cultivated in vitro. Viral RNA from these HERVs has been detected by reverse-transcriptase PCR methods in sera/plasma and brain tissues from MS patients, although not exclusively from these patients [reviewed by Clausen J. Endogenous retroviruses and MS: using ERVs as disease markers. Int MS J. 2003 Apr;10(1):22-8.] Is their activation a cytokine-mediated epiphenomenon, or does it have a pathogenic input into the disease? The many-phased natural history of MS suggests the re-awakening of inherent viruses. Clausen comments: 'preliminary evidence suggests that specific ERVs may act as auto-, super- or neoantigens with the potential to enhance inflammatory responses or induce autoimmune reactions.'

Again, might these inner aliens return to a state of dormancy when the primary cause of cytokine disturbance is removed? It seems likely: we have been living with these beings, their genome trapped within ours, for untold time.

Source: http://www.davidwheldon.co.uk/hhv6.html

ikulo, is there a common denominator to the viruses and bacteria – e.g. HERV, EBV, HV6, Cpn, etc.? I vote for this: they are all a source of inflammation. Inflammation leads to visceral fat; visceral fat leads to cytokines (a.k.a. adipokines); cytokines cause excess insulin production; insulin causes inflammation; and the circle goes round and round.

And in the middle of the cycle, the excess insulin also damages the inside of blood vessels, and it stiffens and thickens smooth muscles and causes general insulin resistance of skeletal muscles.

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My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"

I think it works like this.

The condition to develop MS is prepared by venous insufficiency of the neck veins draining the brains.
This breaks the BBB (in certain areas) and slows all sort of processes important in the vessel walls: feeding, transcription.

If you then get a bacteria outbreak like the Cpn (of which it is known that it may be sleeping in your body for years) or a virus (like EBV also latent), even a vaccination for Hepatitis is suspect, these [or their ligands] will attach to cellular receptors. As these dysfunction, their important role for feeding (cells, ion pump) or transcription (oligodendrocytes that then should compete to maintain the myeline and axons) gets impaired. And if severe enough, you get MS (RR).

But some may 'survive' this first stage of attack, stay reasonably ok and not get MS. But they are not there yet. Because at mid age, the gut comes up. Bacteria in the gut (you have more bacteria in your gut than cells in your body) manipulate T/B cells (the immune system). Some people get diabetes or a rheumatic disorder from this. But our problem is a compromised BBB. And these bad T/B cells are misguided and can get on the myeline. This is the second progressive phase.

In this second phase things like insulin, insulin sensitivity, cytokines, insulin resistance, etc become important.
See for example: http://www.stemcelltherapies.org/multip ... osis_3.htm the paragraph on the leaky gut syndrome
or http://www.kennislink.nl/publicaties/af ... -donorpoep the paragraph on LPS-productie (In Dutch but Google Translate version below)

LPS-producing
Besides the effect on weight Vrieze also examines the influence of intestinal flora on insulin sensitivity. They, inter alia, investigates whether the composition of the intestinal flora influence on the production of lipopolysaccharide (LPS) in the intestine. This substance is released during the fermentation process. LPS, which stimulates inflammatory responses via cytokines, contributes to insulin resistance. Thus the body responds less well to insulin, leading to type 2 diabetes.

Vrieze: "I ​​wonder if the new intestinal flora after the transplantation of poop in lean men also affects the LPS-production and thus on the sugar. If so, then we may have a new target to inhibit the production and type 2 diabetes to address. "