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Important Discovery Exposes Autoimmune Nature of ME/CFS - HERVs Implicated

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by Joel (Snowathlete)

iStock_000022784907_ExtraSmall.jpg

Plasmacytoid dendritic cell interacting with a T-cell.

Some dates you remember forever. Yesterday, on Wednesday 20th February 2013, a paper was published that may represent a major breakthrough in understanding the underlying mechanisms and cause of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS).

The paper, from long-time ME/CFS researchers Dr Kenny De Meirleir, Vincent Lombardi and other colleagues in association with the Whittemore Peterson Institute, reports findings that amount to ME being an autoimmune disease.

Dr Kenny De Meirleir is perhaps best known for the work he has done on the gut and its link to the pathophysiology of ME/CFS, so it is no surprise to hear that this latest finding is related to the major role of the lymphatic immune system in the gut. What will surprise some is that they have been able – despite its massive complexity - to narrow it down to a specific type of cell and to show how this cell ends up creating a state of autoimmunity in the body.

Prompted by reports of associations between other neuroinflammatory diseases and Human Endogenous Retrovirus (HERV) expression, De Meirleir and his team looked for the same type of occurrence in ME/CFS patients. Specifically, they looked in tissue from duodenum biopsies - the duodenum is at the top of the small intestine.


What is being reported?

The paper reports that the Plasmacytoid dendritic cells (pDCs) of eight out of 12 ME/CFS patients studied were found to be immunoreactive to antibodies against HERV proteins. In contrast no immunoreactivity was found in any of the eight controls.

All patients met both the Canadian and Fukuda criteria and were found to have substantial disruption of gut microbiota. Samples were from surplus de-identified clinical biopsies from previous ME patients.

pDCs are part of the innate immune system. They circulate in the blood but occur mostly within the secondary lyphoid organs, which is why they are present in the gut. pDCs are antigen-presenting cells that have a stimulatory role within the immune system. This immunoreactivity to HERV proteins was found uniquely in these pDC cells only. Dendritic cells have the potential to mistakenly identify something as an antigen when they shouldn't, and this may be the cause of some autoimmunity.

HERVs are in our genome. We were born with them, and they are left over viral elements from ancient retroviruses that infected our ancestors' germ line cells millions of years ago and stayed there passively, being replicated and passed on to new generations. They are abundant in our genome (5-8% - Robert Belshaw et al, 2004), but most, probably all, are defective due to mutations and deletions that have occurred in our genome over the millennia. Unlike exogenous retroviruses such as HIV, HERVs are replication incompetent - so they're not a moving target. Our understanding of HERVS is still undergoing change, and there is some evidence that some of this DNA - once thought to be nothing more than junk – actually contributes to our existence by performing various useful tasks within us (J-L Blond et al, 2000). It is known that these HERV elements in our DNA can and do express proteins, though normally they do not provoke a significant immune reaction.

The study reports that proteins found in the ME samples reacted with monoclonal antibodies to HERV proteins and that the immunoreactive cells were pDCs.


What checks did they make?

Positively, having found that the ME patient duoednum tissue was reacting to these HERV antibodies, De Meirleir and his team went a step further and checked to see whether murine retroviral antibodies would also cross react with the tissue - something which should occur if HERV proteins were present - and the results were again positive.

Finally, the team carried out further checks to rule out non-specific reaction and also tested stomach tissue from the same patients and controls, all of which came back negative, as expected.

Now they made efforts to determine exactly which cell types were immunoreactive to the HERV protein antibodies. Via a series of further tests the team hoped to whittle down the potential cell types. First they managed to zoom in on the hematopoietic cell lineage and then further sharpened the result to identify the cells as pDCs. They then double checked via a secondary means to confirm the result.

Having identified that the cells were pDCs, next they counted them and compared that count to the healthy controls. The ME patients were found to have approximately 4.7 times as many pDCs as the controls. Of the pDCs in the duodenum samples from ME patients, approximately 44 percent were found to be reactive to the HERV proteins.

Furthermore, in order to confirm that this was definitely a reaction to identifiable HERV proteins, the team sequenced both the RNA derived from the biopsy samples and from purified pDCs and found matching sequences from known HERVs. Although at this point they cannot definitively rule out that the immunoreaction seen was a result of an infectious exogenous retrovirus, as opposed to a HERV, their identification of matching HERV sequences argues strongly against this possibility.


So the cause of ME/CFS might be autoimmunity to HERVs?

As De Meirleir and his team point out, this would be the first time that an association between pDCs and HERVs has been shown to cause disease, though proven autoimmune diseases such as Multiple Sclerosis and Rheumatoid Arthritis have already been linked with pDC abnormalities and HERV involvement (G Freimanis et al).

The discussion section of the paper suggests that a number of immunological measurements reported in ME/CFS patients in the past, by various groups, may be a result of HERV involvement in pDCs, because pDCs are known to produce a variety of other immunological cells in abundance, such as interferon alpha, which modulates Natural Killer cell (NK) function. Low NK cell function is often associated with ME/CFS (Whiteside TL et al, 1998).

A lot is still unknown about HERVs, but they have been increasingly linked with disease. A study looking at HIV found that HERV expressed peptides were higher in HIV positive patients compared to controls and that T cells responded to these peptides (K E Garrison et al). A pair of studies looking at EBV showed that it could potentially activate retroviral elements in our DNA (Sutkowski et al, 2004 and 1996) and it's possible that something similar could be going on here. Indeed the authors of this paper mention this previous finding and point out the long association between the disease and Herpes viruses, including De Meirleir's previous discovery of herpes viruses in the duodenum of patients with ME/CFS (De Meirleir et al, 2009).

For most of us, immune dysfunction is a hallmark of ME/CFS, and several papers have reported specific immune dysfunction in the disease, particularly in the gut, highlighting the important role that the gut plays in maintaining health. For example, changes in the gut flora can result in incorrect function of the gut mucosal barrier (Shaheen E Lakham et al, 2010). Without these components of the immune system in our gut being correct, we are exposed to increased infection and inflammation and it is thought that this inflammation may be an aggravating factor as there is some evidence of inflammation increasing HERV protein expression and autoimmunity (Lee YK et al, 2011).


What Next?

Replication. That’s what someone (we don’t know who yet) needs to do; someone has to replicate and confirm these findings in a bigger sample of patients. Or disprove them...

We know from experience that we mustn't get ahead of ourselves, and following replication comes more study because it would need to be confirmed that this was the cause of ME/CFS and not some knock-on effect unlinked to the pathogenesis of the disease, but if it checks out then we have a confirmed autoimmune disease and the certainty that goes with it.

We don’t understand autoimmune diseases that well yet, though this finding has the potential to revolutionize our understanding of autoimmunity. If confirmed then these findings could have repercussions for several other autoimmune diseases, particularly those with gastrointestinal dysfunction and neuroinflammation, such as MS, Lupus, and Crohn's, whose cause may follow the same or a similar model. That would be good for everyone. Once again it seems ME/CFS has become sexy, just like it was when the XMRV saga began. Let’s hope this works out better in the long run...

If this research stands up then we are in a great position, because we already understand quite a bit about where the problem is happening. The bad thing about HERVs is that they're immutable - they're in our DNA and we can't do much to change that. On the plus side, everyone has HERVs, so if they are linked with disease then it's important to get to the bottom of how and why, for everybody's sake.

Treatments for autoimmune diseases tend to be immune-modulating drugs to tone down the immune system's effect and limit damage, and initial ‘treatment’ may also involve reducing gut inflammation. The theory is that if you can cut inflammation then you should get less autoimmune reaction, though that alone would be unlikely to fix the problem.

It’s too early to talk about fixes - the first thing we need is for someone to confirm these findings...until then, hold fire...


A Reason to be Hopeful

If it works out then this discovery will be a breakthrough in understanding the cause and mechanisms of ME/CFS. With that reality will come greater recognition, greater funding, greater focus, and ultimately – in the long run – treatments!

Of course none of this will happen overnight, we still have some way to go, but it could mean the beginning of the end, and we have waited for the end to this illness for so long. We deserve this to work out. Don’t we?

But you don’t always get what you deserve. Only time will tell if we remember Wednesday 20th February 2013 as a significant milestone on the long journey we are on to get to the bottom of this illness.



Joel was diagnosed with ME/CFS in 2009 but struggled with the illness for some time prior to this. He loves to write, and hopes to regain enough health to return to the career he loved and have his novels published.



REFERENCES

De Meirleir et al. 2013. Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis Are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins. 2013.

Robert Belshaw et al. Long-term reinfection of the human genome by endogenous retroviruses. 2004

Jean-Luc Blond et al. An Envelope Glycoprotein of the Human Endogenous Retrovirus HERV-W Is Expressed in the Human Placenta and Fuses Cells Expressing the Type D Mammalian Retrovirus Receptor. 2000.

Sutkowski N et al. Epstein-Barr Virus latent membrane protein LMP-2A is sufficient for transactivation of the Human Endogenous Retrovirus HERV-K18 superantigen. Journal of Virology. 2004.

G Freimanis et al. A role for human endogenous retrovirus-K (HML-2) in rheumatoid arthritis: investigating mechanisms of pathogenesis. 2010.

Whiteside TL et al. Natural killer cells and natural killer cell activity in chronic fatigue syndrome. 1998.

K E Garrison et al. T Cell Responses to Human Endogenous Retroviruses in HIV-1 Infection. 2007.

Sutkowski N et al. Virus-encoded superantigens. Microbiological Reviews. 1996.

De Meirleir et al. Detection of herpesviruses and parvovirus B19 in gastric and intestinal mucosa of chronic fatigue syndrome patients. 2009.

Shaheen E Lakhan et al. Gut inflammation in chronic fatigue syndrome. 2010.

Lee YK. Proinflammatory T-cell responses to gut microbiota promote experimental autoimmune encephalomyelitis. 2011.






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Caledonia:
The question that comes to my mind is WHY - we all have HERVs, so why do some people react to them and not others. This is similar to EBV - most people have EBV, so why do some people have reactivations and not others. So this is just another symptom.
Also very small study, and still needs to be replicated.
Not impressed at this time. (Although well written article!)
Hi Caledonia and all,
I do agree with you. Dr.Kenny de Meirleir was invited for a talk to the IAOMT group in Sweden. Researchers and doctors considered afterwards that he was more describing and treating symptoms, than the real cause of ME/CFS. Of course in IAOMT we are prone to blame most symptons on mercury poisoning- but as we think, this is of good reasons. Some PWME´s consulted KDM but had some weird experiences from that. No effect in the long run.
I recall that Rich (vank) told that he had seen more than 200 testresults from Vitamindiagnotics Methylation Panels sent to him from people with ME. All, except a few, showed a decreased methylation and low levels of glutathione. As we can see from the gene tests MTHFR and MTR/MTRR polymorphisms are very common in our group and these gene defects, or one of them, are sufficient to make people vulnerable for a partial methylation blockage.
It will be very interesting to see more of the results from 23and me. I would guess that many will have polymorphisms in the GST genes which means that they propbably can´t make use of their glutathione in a proper way. At least this is what I have seen when I have studied genetest results from Yasko´s Comprehensive Methylation Panel + Genovations genetest, that includes some GST genes, from a group in Sweden diagnosed with ME and mercury poisoning.
If we can´t make glutathione due to decreased methylation , and then can´t make use of the glutathione that we actually have in our bodies, then we can´t detox eg. mercury, mold, toxins from viruses and bacteria in a proper way.
Maybe this is a little of topic in this thread, but I just wanted to explain why we in the IAOMT group in Sweden are very sceptical to KDM´s hypothesis. It would be very interesting to get inputs from you on this.
Helen
 
Yes bad bacteria, but also potentially other pathogens and toxins. There are other people on here with more experience of the gut than me. My own gut is generally good. It was bad at first then got better and the last month has been a little off again, but not as bad as before. I am waiting on test results though as I am told that your gut can be a mess even if you dont get lots of symptoms, so maybe mine is a mess. Dont know yet.
I think the paper is suggesting that the better state you can get your gut in so that it is functioning well and with the minimum of inflammation then the lower your expression of HERV proteins. HERVs aside, as you say, some people have had improvement by getting their gut right so worth trying in that area I think. Like you say though, some people still have problems even if they improve that area. I think as a general rule the longer your illness the worse your chances, but thats just my personal view. I may be wrong about that.
In the case of HERV expression, I dont know if fixing your gut would stop HERV expression altogether, and resolve the immune problem(s), but I think this paper, and other papers talking about HERVs, are saying that you should have less of a problem at least.
I'm going to be paying close attention to my gut test results and trying to improve there in any way I can.

Thanks for answering my questions
 
Yes, they are very very expensive. I suggest you write to them and ask just what you asked me. That is, can there still be a positive with the other tests.

I did the whole set for borrelia, as well as two other infections.

Thanks Helene, will write to them, good suggestion. Did you test positive for both ltt elispot and western blot? Did you also test positive for the two co infections tested? I did cpn and bartonella and was negative for both of these. Many thanks
 
Thanks Helene, will write to them, good suggestion. Did you test positive for both ltt elispot and western blot? Did you also test positive for the two co infections tested? I did cpn and bartonella and was negative for both of these. Many thanks


dear Anniekim, alas, I did test positive for everything I sent in.

But I must be honest, and I have wonder if CFS is not an umbrella for a few comparable conditions, or conversely, is it that all these strange manifestations, borrelia, viral infections are all really one condition. I am having serious trouble with this.


Ps. I note we have another Helen in the thread, so I will just sign off Helene-Canada, don't want my babble mistaken for her lucid texts
 
Hi Caledonia and all,
I do agree with you. Dr.Kenny de Meirleir was invited for a talk to the IAOMT group in Sweden. Researchers and doctors considered afterwards that he was more describing and treating symptoms, than the real cause of ME/CFS. Of course in IAOMT we are prone to blame most symptons on mercury poisoning- but as we think, this is of good reasons. Some PWME´s consulted KDM but had some weird experiences from that. No effect in the long run.
I recall that Rich (vank) told that he had seen more than 200 testresults from Vitamindiagnotics Methylation Panels sent to him from people with ME. All, except a few, showed a decreased methylation and low levels of glutathione. As we can see from the gene tests MTHFR and MTR/MTRR polymorphisms are very common in our group and these gene defects, or one of them, are sufficient to make people vulnerable for a partial methylation blockage.
It will be very interesting to see more of the results from 23and me. I would guess that many will have polymorphisms in the GST genes which means that they propbably can´t make use of their glutathione in a proper way. At least this is what I have seen when I have studied genetest results from Yasko´s Comprehensive Methylation Panel + Genovations genetest, that includes some GST genes, from a group in Sweden diagnosed with ME and mercury poisoning.
If we can´t make glutathione due to decreased methylation , and then can´t make use of the glutathione that we actually have in our bodies, then we can´t detox eg. mercury, mold, toxins from viruses and bacteria in a proper way.
Maybe this is a little of topic in this thread, but I just wanted to explain why we in the IAOMT group in Sweden are very sceptical to KDM´s hypothesis. It would be very interesting to get inputs from you on this.
Helen

Hello Helen,
What you say corresponds to what Rich van K told me after looking at lots of my tests. Glutathione not functioning properly. Rich sent me to KDM, in fact, to address the gut, however, this has not happened as yet.
Cannot eat without pain. Helene-canada
 
Hi Helene-canada :),
My friends who tried treatment by KDM got even more trouble with their guts so they finished. One of them started on Rich´s protocol and is feeling good after one year of treatment - have been sick for 20. (She also removed her amalgam many years ago).

This study might be relevant in this thread:
Clinical activity of folinic acid in patients with chronic fatigue syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/?term=16889122

Joel, thank you very much for your article. I hope you don´t mind my doubts of the trial.

Lansbergen, it is interesting that some of the studies that you link to are about treatment of oral lichen. In Sweden you get free amalgam removal if you have oral lichen. It is stated, they mean, that oral lichen is caused by mercury in amalgam. Maybe they treated a symptom, not a cause in the trials.

In the IAOMT group in Sweden we wished that KDM had noted if his patients had amalgam fillings, or had before.

Helen- sweden
 
Hi Helene-canada :),
My friends who tried treatment by KDM got even more trouble with their guts so they finished. One of them started on Rich´s protocol and is feeling good after one year of treatment - have been sick for 20. (She also removed her amalgam many years ago).

This study might be relevant in this thread:
Clinical activity of folinic acid in patients with chronic fatigue syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/?term=16889122

Joel, thank you very much for your article. I hope you don´t mind my doubts of the trial.

Lansbergen, it is interesting that some of the studies that you link to are about treatment of oral lichen. In Sweden you get free amalgam removal if you have oral lichen. It is stated, they mean, that oral lichen is caused by mercury in amalgam. Maybe they treated a symptom, not a cause in the trials.

In the IAOMT group in Sweden we wished that KDM had noted if his patients had amalgam fillings, or had before.

Helen- sweden

Hello again,
Yes, dear Rich suggested Folinic acid, and I did as he said, with this and Vit b12, but nothing seemed to alter . The dose is not specified there.

I miss Rich very much. He was always willing to adjust things, to help, such a decent man...I just don't know where to turn with him gone.

The other point I wish to make is that for a decade now, I have gone to a variety of CFS specialists,borrelia specialists, and the cardinal problem is that they give a protocol, and then one just goes home and has to try it. The doctor is far, overseas, across the continent. This results in telephone medicine. Ok, so I tried to park myself near the doctor, but that did,not change because he is usually busy sees you for a few minutes, and agin, off you go with try this.

Some folks aren't that sick, and this works, but for delicate constitutions and very sick people there should be a clinic like setting where one is helped and monitored every day for several months.

I looked at evita, but they have no MD doctors there, only naturopaths. The closest I see is Augsburg, but,you do not sleep there.
 
Yes bad bacteria, but also potentially other pathogens and toxins. There are other people on here with more experience of the gut than me. My own gut is generally good. It was bad at first then got better and the last month has been a little off again, but not as bad as before. I am waiting on test results though as I am told that your gut can be a mess even if you dont get lots of symptoms, so maybe mine is a mess. Dont know yet.
I think the paper is suggesting that the better state you can get your gut in so that it is functioning well and with the minimum of inflammation then the lower your expression of HERV proteins. HERVs aside, as you say, some people have had improvement by getting their gut right so worth trying in that area I think. Like you say though, some people still have problems even if they improve that area. I think as a general rule the longer your illness the worse your chances, but thats just my personal view. I may be wrong about that.
In the case of HERV expression, I dont know if fixing your gut would stop HERV expression altogether, and resolve the immune problem(s), but I think this paper, and other papers talking about HERVs, are saying that you should have less of a problem at least.
I'm going to be paying close attention to my gut test results and trying to improve there in any way I can.

Snowathlete, may I ask which gut tests you have recently done? Perhaps cdsa, sibo, leaky gut? Many thanks
 
Joel, thank you very much for your article. I hope you don´t mind my doubts of the trial.
Helen- sweden

Not at all Helen. I welcome a healthy discussion and sharing of views!

Snowathlete, may I ask which gut tests you have recently done? Perhaps cdsa, sibo, leaky gut? Many thanks

I've had the stool test to look for bacteria etc, the redlebs one. Also soluble CD14. I understand this is an indicator of leaky gut. I think it's related to lipopolysaccharide (LPS) in your blood, that can get through your leaky gut, but i dont know much more than that yet.
 
Thanks Helene, will write to them, good suggestion. Did you test positive for both ltt elispot and western blot? Did you also test positive for the two co infections tested? I did cpn and bartonella and was negative for both of these. Many thanks


dear Anniekim, alas, I did test positive for everything I sent in.

But I must be honest, and I have wonder if CFS is not an umbrella for a few comparable conditions, or conversely, is it that all these strange manifestations, borrelia, viral infections are all really one condition. I am having serious trouble with this.


Ps. I note we have another Helen in the thread, so I will just sign off Helene-Canada, don't want my babble mistaken for her lucid texts
" if CFS is not an umbrella for a few comparable conditions"

Most likely so. We have a condition with multiple, somewhat vague definitions each of which circumscribe a wide variety of symptoms. Some of these are specific, such as getting vertigo after acceleration (being passenger in traffic), becoming suddenly knocked out a certain time after exposure to normal heat (hot shower, normal hot outdoor temps), while others, at least in words, describe effects of any debilitating chronic disease.

Fatigue in particular is a misleading term; I've done 180 mile bike rides through hilly country and had nothing like the wipeout delivered by CF/ME/whateveryacallit. It's a sensation more like one's blood draining out.

A more specific list of symptoms may correlate to a specific underlying disease, and we may find several symptom patters which _may_ link to different diseases. We could also be in different stages or manifestations of a common disease.
But right now we only know the effects and have a feel for the causes.

This is definitely a condition of no interest to the lazy of mind. They don't "get it" and never will.
 
you know whats interesting...a couple of months after i got sick, i started having weird gut reactions to food....and also i would go through phases of diarrhea and constipation ..i knew there was something wrong in there but didnt know what. i would wake up with the WORSE imagineable nausea for months. these episodes went on for years.

eventually, the old gut symptoms stopped. but then, i started having HORRIBLE flatulence. and these weren't just any farts......they were so intense and horrid, that my own family would not want to sit beside me anymore. my own mother got up from a bus seat beside me once and changed places!! again, i knew there was something very very wrong inside me but didnt know what.

that went on for several months..maybe a year or 2...i cannot remember....and then it all stopped. now..i KNEW that didn't mean i was better, cuz my CFS was very bad....i kind of felt like, the gut reactions i was having was sort of a good thing - like my body was trying to do something - but it had lost and given up. it couldnt kill the bad bacteria anymore, hence maybe the gases had stopped(?)

then, another strange thing started to happen....my whole back and shoulders started to get cystic acne! this went on for a couple of years..i even went to dermatologists and used topical creams because I could not even sleep sometimes from the painful pustules! i think i still have some scarring.

again, my CFS was getting worse and worse and I knew something very insidious was going on. it was as if the bacteria was going from my gut, right into my bloodstream! my gut could no longer stop it!
 
Re "autoimmune" : how does the very obvious fact(in my cohort anyway) that CFS/ME is Contagious , fit into the HERV implicated theory? I was fine until I was exposed to someone else's really powerful and bad HERV? Because I was just great until that event, after which my life went to hell. So there's an extremely virile contagious HERV out there? and where did it come from? indigenous somewhere? or what. Thanks.


HERVs can be activated by another infection.
this is certainly what happened to me. got a pretty bad "cold", after which i was lactose intolerant. lost my immune system right there. And, as the old saying goes, it was all downhill from there. one thing progressing to the next. will be checking for lymphoma soon, actually asap.
 
Hi Everyone. Not sure what to make of this paper. Other than to say it certainly seems relevent to me presently. Ive always had gut problems. recently had two ( just outside of the colon ) abcesses, and will be haveing a crohns test. I am also suffering from and being tested for bone problems ( possibly inflamation) in my shoulders knees and feet. and recently suspected stomach ulcer. over production of stomach acid. Body aching i would certainly suggest is autoimmune, as might be bowel and stomach problems that i have always had. And are now getting far worse. I will keep everyone updated on the crohns test and the bone investigations. Interesting paper. Autoimmune is a word ive been reading a lot lately with my present problems Hmmm
 
This confirms other studies. The HERV study results from Tufts University are due this year. The current scientific understanding is that certain viruses such as EBV and herpes viruses 1-9 re-activate HERV viruses which are inherited and part of human DNA. These HERV viruses contain super-antigens which cause havoc for the immune system. This leads to chronic activation of the immune system and higher usage of ATP and to total exhaustion of the body.
HERV's are also implicated in AIDS and MS, but they are not the root causes. HERV is a secondary effect of some other attack such as Herpes viruses 1-9 or some other virus which acts as the trigger mechanism.
 
On superantigens and autoimmune disease:

"Autoimmune diseases

It has been proposed that SAgs might contribute to the pathogenesis of autoimmune disease by activating T cells that are specific for self antigens. Although there is no direct evidence of SAg involvement, it has been suggested that SAgs could, under the right conditions, break the tolerance or suppression of auto-reactive T cell clones and induce a state of autoimmunity. Evidence for this hypothesis came from an animal model of multiple sclerosis: experimental autoimmune encephalomyelitis (EAE), where it was shown that administration of SEB to mice recovering from EAE triggered direct stimulation of the Vβ3 positive auto-reactive MBP peptide specific T cells resulting in a rapid relapse of the disease [73,74].
Conrad and colleagues found a biased TcR usage in T cells from IDMM patients towards Vβ7 suggesting the activity of a SAg [58]. They showed that the mitogenic activity was encoded by a gene residing on an endogenous retrovirus, named IDDMK1,222 and that viral expression occurred only in IDMM patients. It was shown later by the same group that IDDMK1,222 is identical to one allele of the EBV-inducible HERV-K18 carrying the Vβ7-specific SAg K18·3 [56] (see above)." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808794/
[my bolding]

I would like to point out though that if we have LPS in the blood, and we have any of the bacteria or viruses that produce superantigens, then superantigens will likely get into our general circulation as well - LPS is a marker of detox failure in my opinion. Staph aureus is the classic superantigen producer, but it is far from alone. Various staph and strep bacteria produce these. Its also worth noting that we tend to have chronic staph or strep nasal infections. Even mycobacteria make them. EBV is thought to have a superantigen.

I am interested in gamma delta T cells due to their super sensitivity to bacterial toxins/markers and their function in suppressing excess immune stimulation. They activate or deactivate the immune system, talk to dendritic cells, and accelerate wound healing.
 
It would seem, most of the degenerative diseases would originate and emanate from the gut, as that is where most of the things enter our body, good and bad. It would also explain why the immune system also evolved mostly in the gut, to deal with this stuff. We should know much more than we do!
 
i agree. no wonder the small and large intestines are supposed to be as big as a football field, if combined and unfolded....and it has been largely ignored all this time! the brain is full of folds too and we hardly know anything about that either.....the gut is like a second brain, they say now.

my doc says "whats there to know? there is bacteria...it digests your food, your nutrients are absorbed, thats about it" WTF!!!
 
Hi to everybody,

I first studied the paper and throw several questions, that I have yet to discuss with some of you to try to solve them. I will also consult with some experts on the subject. Anyhow, and after having "dissected" again the study, I have actually realized that my doubts are actually beyond what it's explained in the paper, in an effort to put together these pieces in order to understand how all this could actually lead to an autoimmune process and finally to the symptoms of CFS.

I have written an article quite similar to that of Joel, in Spanish. I am posting it here for what it may be worth:

http://www.sfc-em-investigacion.com/download/file.php?id=238

There's no need to translate this into English, thanks to the fantastic job Joel and others are doing. However, I enjoyed preparing this drawing in English, and I thought I would share it with you. Maybe some of you can help me out with the interrogation marks I have placed in the sketch, and of course, probably some of you will correct it... It can be funny! ;)

http://www.sfc-em-investigacion.com/download/file.php?id=237&mode=view

Sergio